MYCOVI DNA VIRUS
1. Some General Concepts
Viruses contribute significantly to the global burden of infectious diseases. Most of the diseases are mild, but viruses may cause
severe diseases in susceptible individuals, such as the mal-nourished, immuno-compromised, the very old and the very young.
What is a virus? Very simple structures consisting essentially of a nucleic acid genome, protected by a shell of protein.
May or may not have a lipoprotein envelope.
Has no organelle.
Very small, sizes range 20 - 200 nm, beyond the resolving power of the light microscope.
Metabolically inert and can only replicate inside a host cell.
Genome consists of ONLY one type of nucleic acid; either RNA or DNA.
Viral genome codes for the few proteins necessary for replication: some proteins are non-structural e.g. polymerase, and some are
structural, i.e. form part of the virion structure.
2. Terminology
Virion Infectious virus particle
Capsid Protein shell which surrounds and protects the genome. It is built up of multiple (identical) protein sub-units called capsomers.
Capsids are either icosahedral or tubular in shape.
Nucleocapsid Genome + capsid.
Envelope Lipoprotein membrane which surrounds some viruses, derived from the plasma membrane of the host cell.
Glycoproteins Proteins found in the envelope of the virion; usually glycosylated.
3. Classification of Viruses
Viruses are mainly classified by phenotypic characteristics, such as morphology, nucleic acid type, mode of replication, host
organisms, and the type of disease they cause.
Morphology
Helical morphology is seen in many filamentous and pleomorphic viruses.
Icosahedral morphology is characteristic of many “spherical” viruses.
The number and arrangement of the capsomeres (morphologic subunits of the icosahedron) are useful in identification and classification.
Many viruses also have an outer envelope.
Chemical
Composition
and Mode of
Replication
The genome of a virus may consist of DNA or RNA, which may be single stranded (ss) or double stranded (ds), linear or circular.
The entire genome may occupy either one nucleic acid molecule (monopartite genome) or several nucleic acid segments (multipartite
genome).
The different types of genome necessitate different replication strategies.
Classification of
viruses
A classification places viruses into one of seven groups depending on a combination of their nucleic acid (DNA or RNA), strandedness
(single-stranded or double-stranded), Sense, and method of replication.
Viruses can be placed in one of the seven following groups:
a. dsDNA viruses (e.g. Adenoviruses, Herpesviruses, Poxviruses)
b. ssDNA viruses (+ strand or “sense”) DNA (e.g. Parvoviruses) dsRNA viruses (e.g. Reoviruses)
c. (+)ssRNA viruses (+ strand or sense) RNA (e.g. Picornaviruses, Togaviruses)
d. (−)ssRNA viruses (− strand or antisense) RNA (e.g. Orthomyxoviruses, Rhabdoviruses)
e. ssRNA-RT viruses (+ strand or sense) RNA with DNA intermediate in life-cycle (e.g. Retroviruses)
f. dsDNA-RT viruses (e.g. Hepadnaviruses)
4. Atypical Virus Like Particles
There are four exceptions to the typical virus as described previously:
Defective viruses Composed of viral nucleic acid and proteins, but cannot replicate without a helper virus.
Pseudoviruses Contain host DNA instead of viral DNA.
Viriods Consist of a single molecule of circular RNA with no protein coat or envelope.
Prions Smallest known infectious particles.
Eman K Aldigs*
Medical Microbiology and Parasitology department, King Abdulaziz
University, Jeddah-KSA
*Corresponding author: Eman K. Aldigs, Medical Microbiology and
Parasitology department, King Abdulaziz University, Jeddah-KSA,
Email: ialdoghs@kau.edu.sa
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5. Viral Replication
Viruses are totally dependent on a host cell to replicate. While the sequence and period of events varies somewhat from virus to virus,
the general strategy of replication is similar:
Adsorption
(attachment)
Highly specific, the surface of the virion contains structures that interact receptors on the surface of the host cell. It defines and limits the
host species and type of cell that can be infected by a particular virus. Damage to the binding sites on the virion or blocking by specific
antibodies (neutralization) can render virions non-infectious.
Uptake
(Penetration)
The process whereby the virion enters the cell; as a result of fusion of the viral envelope with the plasma membrane of the cell or
endocytosis.
Uncoating The protein coat of the virion dissociates and the viral genome is released into the cytoplasm.
Early phase Transcription of viral mRNA and translation of a number of non-structural ("early") proteins takes place.
Genome
replication Multiple copies of the viral genome are synthesized by a viral polymerase.
Late phase Transcription and translation of viral mRNA and synthesis of the structural "late" proteins which are needed to make new virions.
Assembly (of new
virions)
The proteins self-assemble and a genome enters each new capsid. This takes place either in the nucleus or in the cytoplasm of the cell,
or sometimes, just beneath the cell surface.
Release of
progeny virions
Release of new infectious virions is the final stage of replication. This may occur either by budding from plasma membrane (for enveloped
viruses), or else by disintegration (lysis) of the infected cell (for non-enveloped viruses). Some viruses use the secretory pathway to exit
the cell.
6. How do Viruses Cause Diseases?
Viruses are capable of infecting all types of living organisms from bacteria to humans.
Cell tropism A major factor that controls which cell type a virus can infect; presence of the appropriate receptor on the cell surface, to which the virus
must attach in order to gain entry into the cell.
Viruses enter the
body
By inhalation, ingestion, sexually, parentral or inoculation through the skin or mucous membranes.
Infection may also sometimes be passed from a mother to her fetus transplacentally (vertical transmission).
Type of infection
May either remain localised to the site of entry, or it may cause a disseminated infection according to the site of target.
Virus replicates initially at the site of entry, but then enters the blood (viraemia) or lymphatics and spreads throughout the body .Other
viruses may replicate locally initially, and then enter nerve endings and travel up the axon to infect the central nervous system.
Incubation period
Time from exposure to an organism to the onset of clinical disease. Viruses that cause localized infections have short incubation periods
(<7 days), while in disseminated infections, the incubation period tends to be longer.
Immune response
Viruses replicate intracellularly, so recovery from a viral infection requires the action of specific cytotoxic T lymphocytes. Virus-specific
antibody levels rise during the course of the infection, but antibody plays only a limited role in recovery. Specific antibodies play a very
important role in preventing reinfection of the host with the same virus.
Certain viruses are able to evade the immune response and establish persistent infections in their host.
7. Viral pathogenesis
Pathogenesis is the process by which an infection leads to disease.
Pathogenic Mechanisms of
Viral Disease
1. Implantation of virus at the portal of entry.
2. Local replication.
3. Spread to target organs (disease sites).
4. Spread to sites of shedding of virus into the environment.
Factors that Affect
Pathogenic Mechanisms
1. Accessibility of virus to tissue.
2. Cell susceptibility to virus multiplication.
Virus susceptibility to host defenses. Natural selection favors the dominance of low-virulence virus strains.
Cellular Pathogenesis
Direct cell damage and death from viral infection may result from:
1. Diversion of the cell’s energy.
2. Shutoff of cell macromolecular synthesis.
3. Competition of viral mRNA for cellular ribosomes.
4. Inhibition of the interferon defense mechanisms.
Indirect cell damage can result from:
1. Integration of the viral genome.
2. Induction of mutations in the host genome.
3. Inflammation.
4. Host immune response.
Tissue Tropism
Viral affinity for specific body tissues is determined by:
1. Cell receptors for virus.
2. Cell transcription factors that recognize viral promoters and enhancer sequences.
3. Ability of the cell to support virus replication.
4. Physical barriers
5. Local temperature, pH, and oxygen tension enzymes and non-specific factors in body secretions.
6. Digestive enzymes and bile in the gastrointestinal tract that may inactivate some viruses.
Implantation at the Portal
of Entry
Virions implant onto living cells mainly via the respiratory, gastrointestinal, skin-penetrating, and genital routes (other routes
can be used). The final outcome of infection may be determined by the dose, location of the virus, infectivity and virulence.
Local Replication and Local
Spread
Most viruses spread among cells extra-cellularly, but some may also spread intra-cellularly. Local infection may lead to localized
disease and localized shedding of virus.
Dissemination from the
Portal of Entry
Viremic: The most common route of systemic spread from the portal of entry is the circulation, which the virus reaches via the
lymphatics. Neural: Dissemination via nerves usually occurs (e.g rabies, herpes and poliovirus).
Multiplication in Target
Organs Depending on the balance between virus and host defenses.
Shedding of Virus Respiratory tract, alimentary tract, urogenital tract and blood are the most frequent sites of shedding, but diverse viruses may
be shed at virtually every site.
Congenital Infections
Infection of the fetus as a target “organ”. The virus must cross additional physical barriers. Transfer of the maternal defenses is
partially blocked by the placenta, the developing first-trimester fetal organs are vulnerable to infection, and hormonal changes
are taking place.
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8. Antivirals
In principle, a molecule can act as an anti-viral drug if it inhibits some stage of the virus replication cycle, without being too toxic to
the body’s cells. The possible modes of action of anti-viral agents would include being able to prevent:
1. Viral attachment and/or entry.
2. Replication of the viral genome.
3. Synthesis of specific viral protein(s).
4. Assembly or release of new infectious virions, or inactivate extracellular virus particles.
5. It must keep in mind that the potential problem of the emergence of mutant virus strains resistant to a drug is always a concern.
Before cell entry
Can be inhibited in two ways:
• Using agents which mimic the virus-associated protein (VAP) and bind to the cellular receptors.
• Using agents which mimic the cellular receptor and bind to the VAP.
Entry inhibitor A number of “entry-inhibiting” or “entry-blocking” drugs are being developed to fight HIV.
Uncoating inhibitor Amantadine and rimantadine, have been introduced to combat influenza. These agents act on penetration/uncoating.
Reverse transcription By developing nucleotide or nucleoside analogues and deactivate the enzymes that synthesize the RNA or DNA once the analogue is
incorporated. This is associated with the inhibition of reverse transcriptase .
Integrase Splices the synthesized DNA into the host cell genome.
Transcription Block attachment of transcription factors to viral DNA.
Translation Based on “antisense” molecules or ribozyme antivirals that have been developed to treat HIV infections.
Protease inhibitors It is used to treat selected patients with HIV infection.
Release phase Two drugs zanamivir (Relenza) and oseltamivir (Tamiflu) that have been introduced to treat influenza prevent the release of viral
particles by blocking a molecule named neuraminidase that is found on the surface of flu viruses.
9. Laboratory Diagnosis
There are four approaches to confirming a viral infection in the laboratory:
• Serology demonstrating an antibody response in a patient’s serum.
• Direct detection of viral antigens in a clinical sample.
• Virus culture.
• Viral nucleic acid detection.
Antibody assays Antibody assays are usually testing by means of the Enzyme-Linked Immune Sorbant Assay (ELISA) technique.
▪ Presence of specific IgM in a single serum sample or a sero-conversion, a rise in titre of specific IgG in paired sera.
Direct demonstration of virus ▪ Electron Microscopy; not a tool that is routinely used to identify viruses in a diagnostic setting.
▪ Demonstration of virus-infected cells in clinical samples by labelled antibodies.
Cultivation Use of laboratory animals, or chick embryos but have largely been replaced by the use of cell monolayers.
Molecular techniques Nucleic acid amplification techniques such as Polymerase Chain Reaction (PCR). It is very sensitive (able to detect only a
few viruses in a clinical sample. Can also be used to measure the amount of virus (viral load) in a patient’s sample.
10. Disinfection and Inactivation of Viruses
A variety of disinfection and inactivation methods are targeted to specific viruses.
Heat Most are inactivated at 56°C for 30 minutes or at 100°C for a few seconds.
Drying Variable; enveloped viruses are rapidly inactivated.
Ultra-violet irradiation Inactivates viruses.
lipid solvents (Chloroform, Ether, Alcohol) Enveloped viruses are inactivated.
Non-enveloped viruses are resistant.
Oxidizing and reducing agents Viruses are inactivated by formaldehyde, chlorine, iodine and hydrogen peroxide.
Phenols Most viruses are resistant.
11. DNA viruses
• Enveloped DNA viruses
• Non-enveloped DNA viruses
Enveloped DNA viruses
Herpesviridae
a. Herpes Simplex Virus 1 (Hsv1)
Case
A 2 years old child with a fever for 2 days was not eating and was crying
often. On examination, the physician noted that the mucous membranes of
the mouth were covered with numerous shallow, pale ulcerations. A few red
papules and blisters were also observed around the border of the lips. The
symptoms worsened over the next five days and then slowly resolved, with
complete healing after two weeks.
My comments:
Key words
Red papules and blisters
Around the border of the lips
Complete healing after two weeks
Facts
HSV1 can cause genital herpes, but most cases of genital herpes are
caused by HSV2.
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Other Considerations
i. Some groups are more likely to have severe, frequent outbreaks and experience complications from herpes if the immune system
is suppressed from:
• HIV or AIDS.
• Chemotherapy for cancer.
• Long term use of high doses of corticosteroids.
• Medications that intentionally suppress the immune system.
ii. Complications of herpes might include:
• Herpes infection in the esophagus.
• Herpes infection of the liver which can lead to cirrhosis (liver failure).
• Encephalitis and/or meningitis.
• Lung infection.
• Eczema herpetiform -- widespread herpes across the skin.
Herpes Simplex Virus 1 (HSV1) /Human Herpesvirus 1
General Characteristics
Linear ds DNA
Icosahedral
Enveloped
Establish latent infection that persists for life
Reservoirs Humans are the only reservoir.
Transmission Direct contact with virus containing body fluids
Diseases
Herpes Labialis - Cold sore
• Painful ulcerating vesicles at the site of initial infection.
• Primarily occurs on the lips and/or the buccal mucosa.
• Spontaneously resolves in < 2 weeks.
• Reactivation of latent HSV-1 in the trigeminal ganglia; Reoccurrence of the painful ulcerating vesicles at the site of initial
infection.
• May also complicate to meningoencephalitis.
Herpetic Keratitis
• Ulcerating vesicles on the cornea.
• May complicate by causing corneal scarring and blindness.
Herpetic Whitlow
• Painful ulcerating vesicles on the cuticles of the Fingernails.
Encephalitis and Meningitis
Pathogenesis The virus spreads to innervating neurons transported to dorsal root ganglia where latency established
Recurrence after reactivation triggered by different factors
Treatment Indirect viral DNA polymerase inhibitors (Acyclovir or Acyclovir pro drugs)
Acyclovir resistant infections are treated with foscarnet.
b. Herpes Simplex Virus 2 (HSV2)
Case
A 23 years old female medical student was told, by clinical exam, that she had
genital herpes four years earlier when she went to student health service for
a sore spot in the area between her vagina and anus. She has had no genital
symptoms since then. She has returned now and wants to know if she really has
genital herpes? What kind? and what to do about it if she has it?! At this visit,
she has no symptoms. An HSV1 and 2 IgG type specific serologic antibody test
is drawn. The result is HSV 1 IgG index value 4.2 and HSV 2 IgG index value
of 0.03. She was given a PCR swab kit to take home and was told if and when
she develops symptoms either orally or genitally that could be herpes (she was
educated about the symptoms), she is to vigorously swab and return the kit to the
clinic to send to the lab.
My comments:
Key words
Genital
Sore spot
Between vagina and anus
Orally
Facts
CDC estimates that 776,000 people in the USA get new herpes
infections annually.
Other Considerations
Pregnancy and HSV2
Pregnant women who are infected with HSV1 or HSV2 have a higher risk of miscarriage, premature labor, slow fetal growth, or
transmission of the herpes infection to the infant during vaginal delivery. Herpes infections in newborns can be life-threatening or cause
disability. Delivery by cesarean section is recommended to avoid infecting the baby.
Herpes Simplex Virus 2 (HSV2)/ Human Herpesvirus 2
Reservoirs Humans (only reservoir)
Transmission
Direct contact
Sexual -Venereal disease
Perinatal
Diseases
Herpes Genitalis
• Painful ulcerating encrustating vesicles at the site of initial infection.
• Primarily occurs on the external genitalia, periorally (if oral intercourse) or perirectally (if anal intercourse).
• Spontaneously resolves in < 2 weeks.
• Reactivation of latent HSV-2 in the lumbosacral paravertebral ganglia; reoccurrence of the painful ulcerating vesicles at the site of
initial infection.
• May also complicate to meningoencephalitis.
Herpetic Keratitis
Herpetic Whitlow
TORCH Syndrome
• Spontaneous abortion, stillbirth, premature birth, birth defects, viral interstitial pneumonitis, acute viral hepatitis leading to jaundice,
hepatosplenomegaly, generalized lymphadenomegaly and neonatal meningoencephalitis leading to mental retardation, seizures,
deafness and blindness.
Treatment Indirect viral DNA polymerase inhibitors (Acyclovir or Acyclovir prodrugs)
Acyclovir resistant infections are treated with foscarnet.
Prevention Barrier contraceptives and safe sex.
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c. Varicella-Zoster Virus (VZV)
Case
18 month old child was presented to emergency room with fever
(39°C), a diffuse rash with some areas showed older crusted lesions
My comments:
Key words
18 month old
Fever
Diffuse rash
Older crusted lesions
Facts
VZV is one of the eight herpes viruses known to infect humans and vertebrates.
Other Considerations
i. The shingles vaccine is not recommended for people who have :
• Had a reaction to gelatin or neomycin.
• A weakened immune system, or have taken drugs to suppress the immune system (such as corticosteroids).
• Tuberculosis.
• A history of lymphatic or bone marrow cancer.
ii. Special Populations
• If immune system is weakened, shingles blisters may spread to other parts of the body and it will likely take longer for the
symptoms to heal. Conditions that weaken immune function include:
• HIV or AIDS.
• Organ transplant recipient.
• Cancer, especially leukemia, Hodgkin’s disease and other lymphomas, or receiving chemotherapy.
• Having an autoimmune disease (like rheumatoid arthritis, lupus, multiple sclerosis, and Crohn’s disease.
Varicella-Zoster Virus (VZV)/ Human Herpesvirus 3
Reservoirs Humans (only reservoir)
Transmission
Direct contact
Respiratory droplet
Contaminated fomites
Diseases
Varicella - “chickenpox” (Primary)
Erythematous ulcerating encrustating vesicles beginning on the face and trunk and then progressing towards the extremities, as well as
mucous membranes
Spontaneously resolves in < 1 week
May complicate to interstitial pneumonitis and meningoencephalitis (primarily occurs in immunocompromized), may progress to zoster
Zoster - “shingles” (Recurrence)
Reoccurrence of the erythematous ulcerating encrustating vesicles on 1 or more dermatomes
Occurs years after initial infection
Caused by reactivation of latent VZV in the paravertebral ganglia
Treatment Indirect viral DNA polymerase inhibitors (Acyclovir or Acyclovir pro drugs)
Acyclovir resistant infections are treated with foscarnet
Prevention In 2006, the United States Food and Drug Administration approved Zostavax for the prevention of shingles
A live attenuated VZV vaccine
d. Epstein - Barr Virus (EBV)
Case
An 18 years old freshman college student presents to the health center complaining
of sore throat and fever for 3 days. She also states that she has been feeling tired
for the past week. On physical exam, she is tired and subdued with a temperature
of 38°C. Her tonsils are enlarged and erythematous. She has enlarged posterior
cervical lymph nodes bilaterally, which are mildly tender to palpation. She has no
supraclavicular, axillary, or inguinal lymphadenopathy. Her spleen tip is palpable
below the left costal margin. A throat swab is obtained to test for group A streptococcal
antigen, which is negative. Laboratory testing reveals a mild leukocytosis with the
presence of atypical lymphocytes. A Monospot test is positive. She declines a course
of corticosteroid therapy. Her symptoms improved in a week.
My comments:
Key words
18 yrs old
Sore throat, fever
Enlarged tonsils
Enlarged posterior cervical lymph nodes bilaterally
Spleen enlargement
Negative for group A streptococcal antigen
Atypical lymphocytes
Positive Monospot test
Facts
EBV, “Kissing disease” affects more than 90 percent of the population
worldwide.
Other considerations
i. Nasopharyngeal carcinoma and Burkitt’s lymphoma are rare, and may not be caused solely by Epstein Barr Virus.
ii. Prevention of Epstein Barr Virus is difficult, because so many adults are already infected with the virus. The virus is spread through
contact with the saliva of an infected person. Since a very large percentage of adults are already infected with the dormant virus, no specific
prevention procedures are recommended by the CDC.
Epstein-Barr Virus (EBV) /Human Herpesvirus 4
Characteristics Latency in B lymphocytes.
Reservoirs Humans (only reservoir)
Transmission Saliva.
Diseases
Infectious Mononucleosis
Fever, headache, severe pharyngitis, splenomegaly and generalized
Lymphadenomegaly.
Spontaneously resolves in < 6 weeks.
Primarily occurs in children and young adults.
EBV infection of the B lymphocytes in the nasopharynx; dissemination of EBV in virtually every lymphoid organ.
May progress to burkitts lymphoma and/or nasopharyngeal carcinoma.
Burkitt Lymphoma
Malignant neoplasm of B lymphocytes.
Primarily occurs in children.
Persistent EBV infection of B lymphocytes.
Nasopharyngeal Carcinoma
Malignant neoplasm of the pharyngeal epithelium.
Primarily occurs in adults.
Reactivation of latent EBV infection of the pharyngeal epithelial cells.
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Treatment None in particular.
Prevention No vaccine available.
e. Cytomegalovirus (CMV)
Case
A 10 month old sarah, presented with loose motions and vomiting since 3 days.
She had 2 episodes of multifocal convulsions 1 month back for which she was
admitted in a private hospital and treated with carbamazepine. A CT brain
was done which showed periventricular calcifications. Her birth was normal.
There was no history of rash or fever in the mother during pregnancy. She
was immunized till age and weaning had been started. On examination, she
had insignificant cervical lymphadenopathy. With persistent loose motions,
she went into septic shock and was treated with IV antibiotics and ionotropic
support. An MRI brain was done which showed extensive nodular calcifications
in periventricular white matter with generalized cerebral atrophy suggestive
of in-utero insult with perimesencephalic vasculopathy suggestive of CMV
infection.
My comments:
Key words
10 month old
Loose motions and vomiting
Multifocal convulsions
Periventricular calcifications in brain
Cervical lymphadenopathy
Septic shock
Extensive nodular calcifications in periventricular white matter
Facts
In the United States, about 30,000 children are born with congenital CMV
infection each year.
Other considerations
• About 1 in 150 children is born with congenital (present at birth) CMV infection; 80% of babies born with congenital CMV infection
never have symptoms or problems.
• About 1 in 750 children in the United States is born with or develops permanent problems due to congenital CMV infection; 5,000
children each year suffer permanent problems caused by CMV infection.
Cytomegalovirus (CMV) /Human Herpesvirus 5
Characteristic Opportunistic pathogen in HIV and AIDS patients
Transmission Direct contact
Perinatal
Diseases
Infectious Mononucleosis-Like Syndrome
Analogous to infectious mononucleosis
May complicate by reactivation of latent CMV in the paravertebral ganglia
Viral interstitial pneumonitis, acute viral hepatitis, and retinitis leading to blindness; primarily occurs in immunocompromised people
TORCH Syndrome/ congenital infection
Treatment Gancyclovir and Valgancyclovir are the drugs of choice
Foscarnet for resistant infections to Gancyclovir.
Prevention Barrier contraceptives and safe sex.
f. Human Herpesvirus 6 (HHV6)
Case
A 18 years old woman was admitted to Hospital with a fifteen day history of
flu-like syndrome. She had been healthy and had a history of self-limiting viral
infections including measles and rubella in childhood. Physical examination
revealed left cervical lymphadenopathy, splenomegaly and sever jaundice.
Abnormal laboratory findings included a white blood cell count of 4.9 ×
109
/L (3% atypical lymphocytes) with large granular cells and anisocytosy in
peripheral smear. Anti-HHV-6 antibody (IgG and IgM) were detected with IgM
index of 3.2 (cut off for positive control > 1.1).
My comments:
Key words
15 day history of flu-like syndrome
Cervical lymphadenopathy
Splenomegaly
Sever jaundice
Facts
Primary HHV6 infection is the most common cause of fever-induced seizures
in children aged 6-24 months.
Other considerations
HHV6 may be associated with various complications such as:
• Encephalitis.
• A possible role in CNS infections and demyelinating conditions.
• May increase the severity of CMV infection in immunocompromised and transplant populations.
• A possible role in lymphoproliferative syndromes.
• HHV6 infection induces bone marrow suppression, respiratory failure, and encephalitis in patients undergoing hematopoietic stem
cell or solid-organ transplantation.
Roseola Virus (HHV6)/ Human Herpesvirus 6
Characteristic Opportunistic virus
Reservoirs Humans (only reservoir)
Transmission Saliva
Diseases
Roseola Infantum - “Exanthema subitum”
High fever and cervical lympadenomegaly
Erythematous rash on the neck and trunk spontaneously resolves in < 1 week.
May complicate by reactivation of latent Roseola Virus in the paravertebral ganglia
Infectious mononucleosis-like syndrome
Viral interstitial pneumonitis, acute viral hepatitis and meningoencephalitis (primarily occurs in immunocompromized)
Primarily occurs in infants
Treatment Indirect viral DNA polymerase inhibitors
Prevention No vaccine available
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g. Kaposi Sarcoma (KS) - Herpesvirus8 (HHV8)
Case
A 32 years old HIV-infected man presents to clinic
having noticed reddish-brown nodular lesions on his
skin. His risk factor for acquisition of HIV is having
sex with other men, his CD4 count is 230 cells/ mm3
,
and he has never taken antiretroviral agents (ART). A
biopsy confirms Kaposi’s sarcoma.
My comments:
Key words
Reddish-brown nodular lesions
HIV
Homosexual
Kaposi’s sarcoma
Facts
Gay and bi-sexual men are more susceptible to infection (through unknown routes of sexual
transmission) whereas the virus is transmitted through non-sexual routes in developing countries.
Other considerations
KS has been divided into several classes essentially by epidemiology;
• Classic KS: Almost exclusively seen in elderly men (possibly due to hormonal factors) of Mediterranean, Middle Eastern or
Eastern European origin.
• Iatrogenic KS: In the 1960s, rare cases of KS began to be reported in people being treated with immunosuppressive drugs, especially
those who had received organ transplants. This form of KS is rarely aggressive and usually goes away once the immunosuppressive
treatment is stopped.
• Endemic or African KS: In east and central Africa described KS as a relatively common, though sometimes much more aggressive
form of classic KS that could also affect children and young adults.
• Epidemic or AIDS-related KS: Follows a variable course, though without ART, it is eventually always progressive.
Kaposi Sarcoma Herpesvirus (KSHV)/ Human Herpesvirus 8
Reservoirs Humans (only reservoir)
Transmission
Direct contact / saliva
Sexual / Semen
Perinatal
Diseases
Kaposi Sarcoma
Malignant neoplasm of vascular smooth muscle – spindle cell tumor
Lesions on skin, face and oral cavity
Treatment None in particular
Prevention No vaccine available
Poxviridae
a. Poxvirus
Case
There were cultures of the smallpox virus in about 70 laboratories around the
world in 1977. In 1978, a photographer in Birmingham, England came down with
smallpox and this was transmitted to her parents. Medical authorities contained
the case and determined that the virus had escaped from a research laboratory
directly below the photographer’s dark room. The researcher responsible for the
small pox virus committed suicide out of guilt. After the escape of the virus from
the research laboratory in England the WHO’s program for the destruction of the
laboratory cultures of smallpox continued until officially there were only two places
where smallpox cultures were held, one in the U.S. and one in the U.S.S.R.
My comments:
Key words
1977
Cultures of smallpox
escaped from a research laboratory
WHO’s program
Two places where smallpox cultures
Facts
The idea of Smallpox vaccination originated in India, as few of the
ancient Sanskrit medical texts described the process of inoculation
Other Considerations
Recent studies suggest that variola and its experimental surrogate, vaccine have a remarkable ability to modify the human immune
response through complex mechanisms that scientists are only just beginning to unravel. Further studies that might require intact virus is
essential. Moreover, modern science now has the capability to recreate smallpox or a smallpox-like organism in the laboratory in addition
to the risk of nature re-creating it as it did once before.
Variola “smallpox”
General Characterstics
Large brick-shaped
Enveloped
dsDNA
Special Characteristics Naturally occurring smallpox was eradicated from 1977
Reservoirs Humans (only reservoir)
Transmission Respiratory droplets
Contaminated fomites
Diseases
“Smallpox”
Fever, chills, headache, backache, and myalgia followed by characteristic rash leaving scars on survivors
Centrifugal distribution of rash
Death results from toxemia and systemic shock
Recovery confers lifelong immunity
Treatment Cidofovir
Vaccinia immune globulins for adverse reactions of vaccine
Prevention A live attenuated vaccine
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b. Molluscum Contagiosum Virus (MCV)
Case
A 48 years old HIV-infected man comes in for routine care and evaluation of
skin lesions on his face. His most recent labs showed a CD4 count of 38 cells/
mm3
and HIV RNA of 87,000 copies/ml. The patient describes a 2-3 month
history of persistent papules on his face that has gradually increased in number
and size. The lesions have not responded to over-the-counter acne therapies.
A clinical diagnosis of molluscum contagiosum is made.
My comments:
Key words
HIV-infected
CD4 count of 38 cells/mm3
and HIV RNA of 87,000 copies/ml
2-3 month history of persistent papules
Facts
MCV is more common in hot climates and with poor hygiene
Other considerations
• Some investigations report that spread of molluscum contagiosum is increased in swimming pools. However, it has not been proved
how or under what circumstances swimming pools might increase spread of the virus. Activities related to swimming might be the cause.
For example, the virus might spread from one person to another if they share a towel or toys. More research is needed to understand if and
for how long the molluscum virus can live in swimming pool water and if such water can infect swimmers.
• Persons with weakened immune systems (such as cancer, organ transplantation, HIV etc.) are at increased risk for catching
molluscum and may develop very large growths (the size at least 15 millimeters in diameter).
Molluscum Contagiosum Virus (MCV)
Characteristics Opportunistic pathogen
Transmission Direct contact
Sexually
Disease Benign nodular skin lesions with no systemic symptoms
Treatment No specific antiviral therapy
Prevention No vaccine available
c. Monkeypox virus
Case
In the Democratic Republic of Congo [DRC]), a 9 years old boy developed
a smallpox like illness showing signs of profuse nasal discharge, ocular
discharge, dyspnea, lymphadenopathy, and mucocutaneous lesions, after
playing with ill prairie dog which was eventually confirmed as human monkey
pox.
My comments:
Key words
Democratic Republic of Congo
9-year-old
Smallpox like illness
Facts
Human cases of an African virus related to smallpox have jumped 20-fold
since 1986.
Other considerations
• Infections of index cases result from direct contact with the blood, bodily fluids, or rashes of infected animals.
• Monkeypox is usually transmitted to humans from rodents, pets, and primates through contact with the animal’s blood or through
a bite.
• Secondary transmission is human-to-human, resulting from close contact with infected respiratory tract excretions, with the skin
lesions of an infected person or with recently contaminated objects. Transmission can also occur by inoculation or via the placenta
(congenital monkeypox).
Monkeypox virus
Characteristics Viral zoonosis
Transmission Close contact with infected mammalian pets
Person to person uncommon
Disease Vesicular and pustular rash differentiated from smallpox by lymphadenopathy
Treatment No specific treatment
Prevention Vaccination with smallpox vaccine
Isolation and infection control guidelines
Non-Enveloped DNA Viruses
Adenoviridae
a. Adenoviruses (HAdV)
Case
A 32-years-old white female with acute onset of left red eye beginning three
days prior thinks her right eye is also becoming involved. Her roommate
had red eyes two weeks prior. She complains of a watery discharge
and her left eye hurts. The left eye has a subconjunctival hemorrhage
overlying generalized conjunctival injection. This hemorrhage results from
inflammation caused by the primary infectious process.
My comments:
Key words
Red eye
Roommate
Watery discharge
Facts
Transmission of adenovirus in recreational waters, primarily inadequately
chlorinated swimming pools, has been documented via faecally-contaminated
water and through droplets.
Other considerations
Health Professionals should;
• Consider adenoviruses as a possible cause of severe pneumonia cases and outbreaks of pneumonia of unknown etiology.
• Adenovirus types 3, 4 and 7 are most commonly associated with acute respiratory disease.
Adenoviruses (HAdV)
014OMICS Group eBooks
Species 50 different human serotypes
General Characteristics
Linear ds DNA
Icosahedral capsid
Non-enveloped
Reservoirs Humans are only reservoir
Transmission
Depending on the syndrome;
Direct contact (“person-to-person”)
Respiratory droplet
Fecal-oral
Contaminated fomites
Diseases
The Common Cold
• Fever, rhinitis leading to rhinorrhea and pharyngitis leading to sore throat
• May complicate by progressing to laryngotracheobronchitis and viral pneumotitis, primarily occurs in children
Keratoconjunctivitis - “Pink eye”
• Keratitis and conjunctivitis leading to conjunctival hyperemia and preauricular lymphadenomegaly
Pharyngoconjunctival Fever
• Fever, rhinitis, pharyngitis, conjunctival hyperemia and preauricular lymphadenomegaly
Gastroenteritis
• Abdominal pain vomiting and watery diarrhea
Treatment Oral fluid and electrolyte replacement in gastroenteritis
Prevention No vaccine available
Hand washing and good infection control practices
Papovaviridae
a. Human Papillomavirus (HPV)
Case
A 32 years old woman who presents for evaluation
after a screening test is positive for Human
Papillomavirus (HPV). She has had sporadic but
negative Papanicolaou (Pap) tests in the past,
with no history of treatment to her cervix.
My comments:
Key words
32 yr old
Screening test
HPV
Negative Pap tests
Facts
Boys and girls at ages 11 or 12 are most likely to have the best protection provided by HPV vaccines, and
their immune response to vaccine is better than older women and men.
Other considerations
Most HPV infections (90%) go away by themselves within two years. But, sometimes, HPV infections will persist and can cause a
variety of serious health problems. Health problems that can be caused by HPV include:
• Genital warts.
• Recurrent Respiratory Papillomatosis (RRP), a rare condition in which warts grow in the throat.
• Cervical cancer.
• Other, less common, but serious cancers, including genital cancers (cancer of the vulva, vagina, penis, or anus), and a type of head
and neck cancer called oropharyngeal cancer (cancer in the back of throat, including the base of the tongue and tonsils).
Human Papilloma Virus (HPV)
General
Characteristics
Circular ds DNA
Icosahedral capsid
Non-enveloped
Reservoirs Humans (only reservoir)
Transmission
Direct contact
Sexual
Perinatal
Contaminated fomites
Diseases
Common Cutaneous Warts - “Verrucae vulgaris”
Painless superficial medium-sized rough hyperkeratinized nodules at the site of initial infection.
Primarily occurs on the hands and fingers as well as on the feet
May progress to deep palmo-plantar warts.
Deep Palmo-Plantar Warts “Myrmecias”
Painful deep medium-sized rough hyperkeratinized pigmented
nodules at the site of initial infection.
Primarily occurs on the feet and toes as well as on the hands
Caused by progression of common cutaneous warts.
Anogenital Warts - “Condyloma acuminata”
Multiple small papules coalescing to form a large cauliflower-like lesion at the site of initial infection.
Primarily occurs on the external genitalia or perirectally (in case of anal intercourse).
Cervical Intraepithelial Neoplasia “CIN”
Benign neoplasm of the cervix
May progress to cervical carcinoma
Cervical Carcinoma
Malignant neoplasm of the cervix
Caused by progression of cervical intraepithelial neoplasia
Treatment Topical liquid nitrogen (if common cutaneous warts, deep palmoplantar warts and/or anogenital warts).
Prevention Two vaccines (Cervarix and Gardasil) protect against cervical cancers. One vaccine (Gardasil) also protects against genital warts
and cancers of the anus, vagina and vulva. Both vaccines are available for females, whereas Gardasil is available for males.
015OMICS Group eBooks
Polyomaviridae
a. Polyomaviruses (JCV and BKV)
Case
A 56 years old male patient of BK-virus nephropathy (BKN) had complications
affecting his renal allografts and causing graft dysfunction. Manifestations included
interstitial nephritis, ureteric stenosis and renal dysfunction. He had a graft loss due
to acute allograft rejection
Patients were diagnosed by the presence of intranuclear viral inclusion bodies in
cells shed in urine and in renal epithelial cells (‘decoy cells’). Molecular diagnosis
based on real-time Quantitative Polymerase Chain Reaction (Q-PCR) on urine/
blood strengthens the suspicion. Final diagnosis was made by specific findings in the
allograft biopsy, in particular positive immunohistochemical staining for viral proteins
My comments:
Key words
BK-virus nephropathy
Acute allograft rejection
Facts
For nearly 40 years, only two plyomaviruses were known to infect
humans. Genome sequencing technologies have recently discovered
seven additional human polyomaviruses, including one causing most
cases of Merkel cell carcinoma and another associated with Transplant-
Associated Dysplasia (TSV)
Other considerations
Merkel Cell Polyomavirus (MCV or MCPyV) was first described in January 2008. It is suspected to cause the majority of cases of
Merkel cell carcinoma, a rare but aggressive form of skin cancer. Approximately 80% of Merkel cell carcinoma (MCC) tumors have been
found to be infected with MCV. MCV appears to be a common infection of older children and adults. It is found in respiratory secretions
suggesting that it may be transmitted by a respiratory route. But it also can be found shedding from healthy skin, and in gastrointestinal
tract tissues and elsewhere, and so its precise mode of transmission remains unknown.
Polyomaviruses (JCV and BKV)
General
Characteristics
Circular ds DNA
Icosahedral capsid
Small
Non-enveloped
Special
Characteristics
Persist as latent infections in a host without causing disease
May produce tumor (Oncogenic)
Reservoirs Humans (only reservoir)
Transmission The mechanism of human-to-human transmission of the polyomaviruses JC virus (JCV) and BK Virus (BKV) has not
been firmly established
Diseases
Highly common childhood and young adult infections mostly cause little or no symptoms. Lifelong persistence among
almost all adults
Most common among persons who become immunosuppressed by AIDS, old age or after transplantation and include
Merkel cell carcinoma, PML and BK nephropathy
Progressive multifocal leukoencephalopathy caused by reactivation of JC virus
Nephropathy and Merkel cell cancer (Merkel cell virus) caused by reactivation of BK virus
Treatment No known treatment
Prevention Non available
Parvoviridae
a. Human Parvovirus B19
Case
A kidney transplant recipient, was unresponsive to treatment of severe anemia,
and presented hypocellular hematopoietic marrow, megaloblastosis and
hypoplasia of erythroid lineage with larger cells with clear nuclei chromatin and
eosinophilic nuclear inclusions. This patient was seropositive for Epstein-Barr
and Cytomegalovirus infections and negative for anti-parvovirus B19 IgM and
IgG antibodies, although symptoms were suggestive of parvoviruses infection.
A qualitative polymerase chain reaction testing for B19 in serum sample
revealed positive results for B19 virus DNA.
Key words
Kidney transplant recipient
Unresponsive to treatment
Seropositive for EBV and CMV
PCR positive for B19
Fact
People with fifth disease are most contagious before they get rash or joint pain
and swelling.
Other considerations
At the moment, there are no treatments that directly target the Parvovirus B19 virus. Intravenous Immunoglobulin Therapy (IVIG)
therapy has been a popular alternative because doctors can administer it without stopping chemotherapy drugs like MEL-ASCT. Also,
the treatment’s side effects are rare as only 4 out of 133 patients had complications (2 had acute renal failure and 2 had pulmonary edema)
even though 69 of the patients had organ transplants and 39 of them were HIV positive. This is a large improvement over administering
Rituximab. The monoclonal antibody against the CD20 protein has been shown to cause acute hepatitis, neutropenia via Parvovirus B19
reactivations, and even persistent Parvovirus B19 infection. However, it is important to note that IVIG therapy is not perfect as 34% of
treated patients will have a relapse after 4 months.
Human Parvovirus B19
General Characteristics
Linear ss DNA
Icosahedral capsid
Non-enveloped
Reservoirs Humans
Transmission
Direct contact
Perinatal
Parenteral
Diseases
Erythema Infectiosum - “slapped-cheek disease”
Erythematous rashes of the cheeks as well as on the trunk and extremities.
May complicate by infection of the bone marrow, aplastic anemia, transient aplastic crisis (primarily occurs in infants,
immunocompromized or if already anemic)
Spontaneously resolves in < 1 week
Primarily occurs in children
Treatment None in particular.
Prevention Not available.
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Hepatitis Viruses
• Enterical transmitted hepatitis viruses, I (HAV, HEV)
• Parentral transmitted hepatitis viruses, II (HBV, HDV, HCV and HGV)
Enterical Transmitted Hepatitis Viruses, I (HAV, HEV)
a. Hepatitis A Viruses (HAV) - Picornaviridae
Case
In July 2013, 134 people have been confirmed to have hepatitis A after eating
“Townsend Farms Organic Antioxidant Blend” in 8 US states.
My comments:
Key words
134 people
8 states
Eating
Facts
• Globally, there are an estimated 1.4 million cases of hepatitis A every year.
Other considerations
• Hepatitis A virus infection can be prevented if a person has been exposed to the Hepatitis A virus from contaminated food or water.
If the exposure occurred within the last 14 days, a dose of Hepatitis A vaccine or Immunglobulin (IG) can prevent illness. Vaccination
after 14 days is not believed to help prevent a person from getting hepatitis A.
• Vaccine is used to prevent Hepatitis A virus infection from contaminated food or water; which depends upon a person’s age and
health status.
• Two different shots may be used: the hepatitis A vaccine and Immunglobulin (IG). Persons who are Immunocompromised, with
chronic liver disease, and for whom Hepatitis A vaccine is contraindicated should receive immunglobulin.
Hepatitis A Virus (HAV)
General
Characteristics
Linear positive-sense (does not need a viral RNA-dependent RNA
Polymerase to replicate) ss RNA
Icosahedral capsid
Non-enveloped
Special
Characteristic Epidemic infectious hepatitis
Reservoirs Humans
Animals (primarily primates)
Transmission
Direct contact
Fecal-oral
Contaminated water and food (primarily seafood)
Diseases
Acute Viral Hepatitis
Moderate hepatic damage
Fever, abdominal pain, vomiting, hepatomegaly and jaundice
Spontaneously resolves in < 3 months
Treatment None in particular
Prevention
A formalin- inactivated HAV vaccine for travelers
Passive immunization with HAV immunoglobulin for post exposure prophylaxis
Hand washing
b. Hepatitis E Virus (HEV) - Caliciviridae
Case
During 2011, 5 persons in Lazio, Italy were infected with a strain of Hepatitis E
virus that showed high sequence homology with isolates from swine in China.
Detection of this genotype in Italy parallels findings in other countries in Europe.
My comments:
Key words
5 persons
Strain
Genotype
Facts
• Every year there are 20 million hepatitis E infections, over three million
acute cases of hepatitis E, and 57 000 hepatitis E-related deaths.
Other considerations
• Hepatitis E is most common in developing countries with inadequate water supply and environmental sanitation. Large hepatitis E
epidemics have been reported in Asia, the Middle East, Africa, and Central America.
• People living in refugee camps or overcrowded temporary housing after natural disasters can be particularly at risk.
• The unique characteristic of HEV is displaying different epidemiological and clinical characteristics between developing and
developed countries.
• Hepatitis E virus is spread by animals: there is a possibility of zoonotic spread of the virus. HEV RNA had been extracted from meat
and organ of some animal species including pigs, boar, and deer. Food borne infection could occur from consumption of uncooked/
undercooked products from infected animals.
Hepatitis E Virus (HEV)
General
Characteristics
Linear (+) ss RNA
Icosahedral capsid
Non-enveloped
Special
Characteristics Same diseases and treatment as HAV
Reservoirs Humans
Animals (primarily primates, swine and rodents)
Transmission Fecal-oral
Contaminated water
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Diseases
Acute Viral Hepatitis
Moderate hepatic damage
Fever, abdominal pain, vomiting, hepatomegaly and jaundice
Spontaneously resolves in < 3 months
Treatment None in particular
Prevention
No vaccine is available for HEV infection to date
Improved sanitary lower transmission rate
Travelers to endemic areas should be cautioned about contaminated water
Parenteral Transmitted Hepatitis Viruses, II (HBV, HDV, HCV and HGV)
a. Hepatitis B Virus (HBV) - Hepednaviridae
Case
The patient is 24 years old who has recently passed her third year in dental
school. She is HBsAg (+), HBeAg (+), anti-HBe (-). Her HBV DNA is 400
million copies/mL (approximately 80 million int. unit/mL) and serum ALT is 45
(upper limit of normal 40 int. unit/L). Her liver biopsy shows macrovesicular
fat, no portal fibrosis.
My comments:
Key words
Dentist
HBsAg (+), HBeAg (+), anti-HBe (-)
400 million copies/mL
Serum ALT is 45
Facts
One third of the world’s population has been infected with the hepatitis B virus
Other considerations
Vaccination is recommended for certain groups, including:
• Anyone having sex with an infected partner or people with multiple sex partners.
• Anyone with a sexually transmitted disease.
• Men who have sexual encounters with other men.
• People who inject drugs.
• People who live with someone with Hepatitis B.
• People with chronic liver disease, end stage renal disease, or HIV infection.
• Healthcare and public safety workers exposed to blood.
• Travelers to certain countries.
• All infants at birth.
Hepatitis B Virus (HBV)
Characteristics
Circular ds DNA
Icosahedral capsid
Enveloped
Reservoirs Humans (only reservoir)
Transmission
Direct contact (saliva, skin lesions, body fluids)
Sexual
Perinatal
Parenteral
Diseases
Acute Viral Hepatitis
May progress to hyperacute viral hepatitis.
Hyperacute Viral Hepatitis - “fulminant hepatitis”
Severe hepatic damage
Hepatic failure leading to generalized edema, ascites, coagulopathies and hepatic encephalopathy
Primarily occurs in immunoreactive
Chronic Persistent Viral Hepatitis
Moderate hepatic cirrhosis
Fever, abdominal pain, vomiting, hepatomegaly and jaundice
Primarily occurs in moderately immunocompromised
May progress to chronic aggressive viral hepatitis
Chronic Aggressive Viral Hepatitis
Severe hepatic cirrhosis and Hepatic failure
Primarily occurs in severely immunocompromised
Chronic Carrier State
No hepatic damage and no hepatic cirrhosis (asymptomatic)
Hepatocellular Carcinoma
Malignant neoplasm of the hepatocytes
Diagnosis
Biochemical tests + serologic assays
IgM antibody to HBcAg indicates acute infection
Antibody to to HBsAg indicates immunity to HBV
Treatment Chronic HBV is treated with interferon-alpha, lamivudine or adefovir
Prevention
Recombinant HBsAg vaccine
Passive immunization with HBV immune globulin to neonates born to HBsAg (+) mothers and after needlestick exposure
Avoid high risk behavior
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b. Hepatitis D Virus (HDV) - Deltaviridae
Case
Seven patients with Hepatitis Delta Virus (HDV) cirrhosis underwent liver
transplantation. In every case the HDV infection was florid but accompanied by an
inactive Hepatitis B Virus (HBV) infection. The patients were given Anti-HB Surface
Antigen (HBsAg) serum globulins and HBV vaccine. Two patients cleared the
HBsAg and the HDV, and are alive and well 14 and 15 months, respectively, after
transplantation. HDV infection recurred in the other five patients: hepatitis developed
in three, another died, and the fifth was re-transplanted for cause’s unrelated to viral
hepatitis (reinfection was shown by the presence of HD antigen in the graft). Liver
transplantation is feasible in patients with HDV disease but involves a high risk of
HDV reinfection that cannot be predicted by the virological pattern of the native HBV
infection or prevented by conventional HBV prophylaxis.
My comments:
Key words
HDV
Cirrhosis
Liver transplantation
Inactive HBV
HBsAg serum globulins and HBV vaccine
Facts
Severe often fatal acute and chronic HDV is among indigenous
people of Venezuela, Colombia, Brazil and Peru
Other considerations
i. Two epidemiological patterns of HDV infection exists;
• In Mediterranean countries infection is endemic among HBV carriers, and is transmitted by close personal contact.
• In Western Europe and North America, HDV is confined to persons exposed to blood or blood products, e.g. intravenous drug
addicts sharing unsterilized injection needles.
ii. New foci high HDV prevalence continues to be identified as in the case of island of Okinawa in Japan, areas in China, North India
and Albania.
Hepatitis D Virus (HDV)
General Characteristics
Linear negative-sense ss RNA (needs a viral RNA-dependent RNA polymerase to replicate)
Icosahedral capsid
Non-enveloped (needs HBV envelope to become infective)
Special Characteristics Same reservoirs, transmission and diseases as HBV
Treatment None in particular
Prevention HBsAg vaccine
c. Hepatitis C Virus (HCV) - Flaviviridae
Case
A prominent former doctor and endoscopy clinic owner was convicted of 27 criminal
charges including second-degree murder in a hepatitis C outbreak. Endoscopy clinic
nurse-anesthetist was found guilty for 16 of 27 charges against him. The murder
conviction stemmed from the death of 77-year-old patient was visiting the clinic.
My comments:
Key words
Endoscopy clinic
Hepatitis outbreak
Nurse-anesthetist
77yr old died
Facts
~3% of the world’s population is living with chronic hepatitis C.
Egypt has high rates (14.7%) of infection.
Other considerations
Early diagnosis can prevent health problems that may result from infection and prevent transmission to family members and other
close contacts. Some countries recommend screening for people who may be at risk for infection. These include:
• Current or former injecting drug users (even those who injected drugs once many years ago.
• People on long-term haemodialysis.
• Health-care workers.
• People living with HIV.
• People with abnormal liver tests or liver disease.
• Infants born to infected mothers.
• 12-24 hours after needle exposure.
Hepatitis C Virus (HCV)
General Characteristics
Linear negative-sense ss RNA (needs a viral RNA-dependent RNA polymerase to replicate)
Icosahedral capsid
Non-enveloped (needs HBV envelope to become infective)
Special Characteristics Same reservoirs, transmission and diseases as HBV
Reservoirs Humans (only reservoir)
Transmission
Direct contact (saliva, skin lesions, body fluids)
Perinatal
Sexual and Parenteral (not confirmed)
Treatment A combination of interferon-alpha and ribavirin for chronic HCV hepatitis
Prevention No vaccine available
Screening blood products and avoiding intravenous drug use
Hepatitis G Virus (HGV)
Characteristics Same reservoirs and transmission as HBV
Diseases None directly associated
Treatment None in particular
Prevention No vaccine available.
Screening blood products and avoiding intravenous drug use