Virology Final Exam Review

Characteristics of All Viruses

\-viruses are not living

\-they have to be infectious to endure in nature (survive)

\-viruses must be able to use host cell processes to produce their components (viral mRNA, protein, identical copies of the genome)

\-must encode any required process not provided by the cell

\-viral components have to self-assemble

Defective Viruses

viruses which lack a complete genome, so they cannot completely replicate or form a protein coat

\
\-can replicate only when their genetic defect is complemented by a helper virus

Abortive Infections

failed infections of a cell

Non-Permissive Cells

host cells that will not allow replication of a particular type or strain of virus

Permissive Cells

host cells that provide the biosynthetic machinery the virus needs to complete it its replication cycle

Cells in Culture

\-animal cells in culture are derived from living animal tissue

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\-%%adherent cell culture: cells need contact with solid surface for division (anchorage dependent)%%

\-%%suspension cell culture: cells are suspended in a medium (ex. agar)%%

Types of Cells in Cell Culture

\-%%primary cells:%% cells taken from a living animal or human person (ex vivo)

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\-%%continuous cell lines:%% population of cells that can be grown/divide in culture indefinitely; immortal

* continue to express telomerase activity = elongating telomeres
* a type of continuous cell line; group of stem cells (self-renewing) that is cultured in vitro and can be propagated indefinitely

In vitro

cell culture maintenance on glass

In vivo

experiments in live animals, not cell cultures

in humans = clinical translational research

Ex vivo

cell culture using cells taken from a living animal or human person

The Cell Cycle

\-Interphase: period during which cells grow

* G1: growth
* \*G0: the cell is just doing its job
* S: DNA synthesis
* G2: growth and preparation for mitosis

\-Mitosis: period during which a cell divides into two daughter cells

G0 Phase

within the G1 phase; serum deprivation stops protein synthesis and thus, cell proliferation; cell growth arrest

G1 Checkpoint

control mechanism that ensures everything is ready for DNA synthesis

G2 Checkpoint

control mechanisms that ensures everything is ready to enter the M phase and divide

M Checkpoint

control mechanism that ensures the cell is ready to start cell division

Viruses have the greatest…?

genetic diversity in nature

\-%%Viral genome modification processes: mutation, recombination, and reassortment%%

* increase genome variability
* natural selection decides if these changes in the viral genome will promote survival; if lethal changes result, virus will disappear; if beneficial changes result, trait will be fixed in the genome

Viral Mutations

can be spontaneous, induced, or engineered

Spontaneous Mutations

\-due to mistakes in the normal replication of viral nucleic acid

\*accumulate in viral genomes and introduce variations in phenotypes that are subjected to selection pressure during evolution

\*%%mutation rates much higher in RNA viruses than DNA viruses because of lack of proofreading activity in RNA replication enzymes%%

* %%Ex. influenza, you have to get a new vaccine every year%%

Class I

double-stranded DNA (+/-)

Class II

single-stranded DNA (+)

%%-ssDNA → dsDNA → mRNA strand%%

Class III

double-stranded RNA (+/-)

@@Class IV@@

single-stranded RNA (+)

RNA (-)?

Class V

single-stranded RNA (-)

Class VI

single-stranded RNA (+)

\-reverse transcribing virus %%(retrovirus)%%

Class VII

double-stranded DNA (+/-)

\-reverse transcribing virus

DNA Viruses

\-virus that has a genome made of DNA that is replicated by a DNA polymerase

\-genome is replicated by either host or virally encoded DNA polymerases

\-stability of DNA allows for genomes to be much larger than RNA viruses

\-mostly replicate in the nucleus, except for Poxvirus

Class I dsDNA Virus Families

\-Adenoviridae (human adenovirus C, respiratory disease)

\-Herpesviridae (varicella zoster virus, chickenpox)

\-Papillomaviridae (HPV, warts, cervical cancer)

\-Polyomaviridae (JC virus, PML)

\-Poxviridae (variola virus, smallpox)

Class II ssDNA Virus Family

Parvoviridae (parvovirus, B19 fifth disease)

Class VII Viruses Families

\-dsDNA/RNA

\-Hepadnaviridae (hepatitis B)

RNA Viruses

\-RNA is labile and transient (DNA is not)

\-most replicate in the cytoplasm

\-RNA viruses must encode an RNA-dependent RNA polymerase because host cells can’t replicate RNA

\-genome structure determines mechanisms of transcription and replication

\-highly prone to mutations and lack proofreading activity

\-make up majority of human viral pathogens

Positive RNA Viruses

\-Picornaviruses: polio, common cold, Hepatitis A

\-Togaviruses: rubella

\-Flaviviruses: yellow fever, hepatitis C, dengue fever

\-Coronaviruses: COVID, SARS, MERS, common cold

Negative RNA Viruses

\-Paramyxoviruses: measles, mumps

\-Rhabdoviruses: rabies

\-Orthomyxoviruses: influenza

\-Bunyaviruses: respiratory distress hemorrhagic fevers

RNA Retroviruses

\-HTLV

\-HIV (carry reverse transcriptase within the viral particle)

\
\-Reverse Transcriptase = RNA-dependent DNA polymerase that makes DNA intermediate

\-First retrovirus discovered: Rous sarcoma virus (Peyton Rous, 1910)

* oncogene = src

\-First human retrovirus case = two patients w/ T cell lymphomas (HTLV-I, human T lymphotropic virus), 1978

\-HIV/AIDS discovered 1983

Double-Stranded RNA Viruses

\-Reoviruses: respiratory and gastrointestinal infections

Detection of Viral Proteins

detect:

\-protein patterns w/ electrophoresis

\-enzyme activities

\-hemagglutination and hemadsorption

\-antigen detection (ELISA, western blot, immunofluorescence, antigen rapid tests)

Detection of Viral Nucleic Acids

\-Restriction endonuclease cleavage patterns

\-Electrophoresis (segmented RNA viruses)

\-DNA genome hybridization (*in situ* hybridization)

\-Southern, Northern, and dot blots

\-Polymerase chain reaction (PCR, RT-PCR)

Immunofluorescence

\-%%Direct: fluorochrome labeled antibody directly binds to the target tissue antigen%%

\-%%Indirect: an unlabeled antibody binds to the target tissue antigen, then a fluorochrome labeled antibody (anti-Ig) against the unlabeled antibody binds%%

* stronger signal than direct

Type I Interferon

Type I IFN: %%cytokines which play essential roles in inflammation, immunoregulation, tumor cell recognition and T cell responses%%

* bind specific cell surface receptor complex on target cells called IFN-a/B; %%leads to expression of proteins that will prevent the virus from producing and replicating its RNA and DNA%%


* produced when the body recognizes that a virus has invaded it (recognition of viral components like nucleic acids)
* induced in virtually all cell types upon recognition of viral components

Type II Interferon

\-IFN y in humans

\-%%known as the immune IFN, activated by interleukin-12%%

\-%%released by cytotoxic T cells (CD8) and type-1 T helper cells (TH1 CD4)%%

\-induced by cytokines like IL-12; %%expression restricted to immune cells%% like T cells, NK cells, macrophages, and dendritic cells

Modes of Transmission of Communicable Diseases

Direct:

\-horizontal contact (ex. kissing, sex)

\-airborne droplets between people (ex. sneezing, coughing)

\-vertical contact (through pregnancy, birth canal)

\-disease vectors

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Indirect:

\-contact with fomites

\-fecal-oral contamination

\-food, water, biological products

\-airborne (ex. soil that has been kicked up)

Inapparent Infection

presence of infection in a host without occurrence of recognizable clinical signs or symptoms

Acute Infection

\-localized infection: infection remains in one specific area or organ

\-generalized infection: infection spreads across the body

\-congenital infection: caused by viruses that may be picked up by the baby at any time during the pregnancy up through the time of delivery

Persistent Infection

virus is not cleared but remains in specific cells of infected individuals; virus may become latent and stay in the body

Transformation Infection

change in growth, phenotype, or indefinite reproduction of cells caused by the introduction of inheritable material. Through this process, a virus causes harmful transformations of an in vivo cell or cell culture.

Characteristics of Antiviral Agents

%%Desirable:%%

\-metabolic stability

\-ready to transport to infected target organs

\-chemical and thermal stability

\-good solubility at or close to physiologic pH

\-low cost of preparation

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%%Undesirable:%%

\-causes acute toxicity

\-causes chronic pathogenesis effects

* teratogenesis: congenital malformations
* mutagenesis: DNA may experience physical changes that induce mutations
* carcinogenesis: cause cancer

\-immunosuppressive

\-incorporates into DNA of the noninfected cell

\-develops into resistant mutant

\-causes activation of latent viruses

Types of Immunity

Viral Escape Mechanisms

\-poor or absent immune response to pathogen

\-intercellular spread of viruses

\-rapid changes in antigenic composition of some viruses

\-genetically determined susceptibility

\-growth of viruses on lymphoretiuclar cells

\-viral induced immunosuppression

\-antibody modulation of virus antigens on cells

\-viral latency

\-mimicry of host cell’s molecules or ligands

\-hiding their binding sites from antibodies

\-virokines

Types of Viral Vaccines

\-inactivated vaccines

\-live attenuated vaccines

\-recombinant vaccines

\-subviral particle vaccines

\-anti-idiotypic vaccines

Picornaviruses

\-%%positive, single-stranded RNA genome%%

\-%%naked, small, icosahedral capsid%%

\-Enteroviruses are resistant to pH 3 to 9, detergents, mild sewage treatment, and heat

\-Rhinoviruses are labile at acidic pH; optimum growth temperature is 33 degrees Celsius

\-%%replicates in cytoplasm%%

\-%%viruses are cytolytic%% (get out by breaking the host cell)

Togaviruses

\-%%positive, single-stranded RNA genome%%

\-%%enveloped, non-segmented%%

\-@@Alphaviruses@@

* @@transmitted by arthropods (arthropod borne = arboviruses)@@
* 27 known, 11 cause disease in humans

\-@@Rubivirus = causes rubella@@

Flaviviruses

\-%%positive, single-stranded RNA genome%%

\-%%enveloped, non-segmented%%

\-%%causes anywhere from febrile illnesses to life-threatening hemorrhagic fevers, encephalitis, and hepatitis (hep C)%%

\-70 types, 13 infect humans

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Some of the Most Important Viral Pathogens in Developing World:

\-@@yellow fever@@

\-@@dengue fever@@

\-Japanese encephalitis

\-St. Louis encephalitis

Bunyaviruses

\-%%negative, single-stranded RNA genome%%

* %%half positive and half negative RNA strands (ambisense)%%

\-%%enveloped, segmented%%

\-most are arboviruses (spread by mosquitoes, ticks, or flies)

* endemic to the environment of the vector

\-at least 200 exist

Parts of the Virus

\-hemagglutinin: glycoproteins on surface of the cell important for binding

\-neuraminidase: enables the virus to be released from the host cell; on surface of the cell

\-matrix protein

\-lipid bilayer

\-polymerase

\-nucleoprotein: proteins conjugated with nucleic acids (either DNA or RNA);typical nucleoproteins include ribosomes, nucleosomes and viral nucleocapsid proteins

\-RNA

Influenza Antigenic Drifts and Shifts

Drifts: little mutations that occur in the virus; overtime the accumulation of these mutations makes the virus a completely different thing

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Shifts: recombination between two different influenza viruses that are coinfecting a species cause significant changes that create a new virus species; occur in less than a year

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\*influenza viruses change so quickly because of these types of mutations

Influenza Strains Nomenclature

\-%%Type%%

\-%%Host of origin%%

\-%%Geographic origin%%

\-%%Strain number%%

\-%%Year of isolation%%

\-%%Antigenic descriptions%%

Diseases Associated with Influenza Virus Infection

%%Influenza in Adults:%%

\-rapid onset fever

\-malaise

\-myalgia

\-sore throat

\-nonproductive cough

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%%Influenza in Children:%%

\-acute disease similar to adults

\-higher fever

\-gastrointestinal symptoms (abdominal pain, vomiting)

\-otitis media

\-myositis

\-croup

Influenza Modes of Control

\-vaccines with predicted yearly strains of influenza A and B viruses

* @@important vaccine = neuraminidase vaccine@@

\-several antiviral treatments have been approved against influenza for prophylaxis or early treatment

Coronaviruses

\-%%large, positive, single-stranded RNA genome%%

\-%%enveloped, non-segmented%%

* studded with long petal-shaped spikes

\-nucleocapsids are long, flexible helices

\-%%second most frequent etiologic agents of common cold in US%%

\-%%causative agent of severe acute respiratory syndrome (SARS-COV1)%% that emerged in Asia in winter of 2002 and Middle East respiratory syndrome (MERS) first reported in 2012

\-play a role in some human enteric infections

\-could also cause viral pneumonia and myocarditis

Coronavirus Pandemic

\-SARS-COV2 appeared in Wuhan, China in 2019

\-COVID-19 disease

%%-USA: 105,394,979 cases, about 1.2 million deaths (1,146,735 deaths)%%

\-%%Global: 674,622,359 cases, about 6.9 million deaths (6,875,314 deaths)%%

Vaccine and Treatments Against COVID-19 Approved in USA

Vaccines:

\-Pfizer = mRNA vaccine

\-Moderna = mRNA vaccine

\-Johnson & Johnson = a DNA vaccine

\
Treatments

\-Remdesivir and other antiviral FDA approved drugs

\-monoclonal antibody treatments

Orthomyxoviruses

\-%%negative, single-stranded RNA genome%%

\-%%enveloped, segmented%%

\-influenza A, B, and C viruses

Paramyxoviruses

\-%%single-stranded, negative RNA genome%%

\-%%enveloped, non-segmented%%

\-mumps (1 serotype)

\-measles (1 serotype)

\-parainfluenza 1-5 (5 serotypes)

\-respiratory syncytial virus (2 serotypes)

Paramyxoviruses: Spread of Mumps

1. Inoculation of respiratory tract
2. Local replication
3. Viremia
4. Systemic infection around various parts of the body (in image)

Paramyxoviruses: Spread of Measles

1. Inoculation of respiratory tract
2. Local replication in respiratory tract
3. Lymphatic spread
4. Viremia
5. Wide dissemination to different parts of the body (view image)

Koplik spots and exanthem are diagnostic indicators of?

measles (NOT rubella)

\-small, white spots (often on a reddened background) that occur on the inside of the cheeks

@@Respiratory Syncytial Virus Proteins@@

\*

Clinical Consequences of Respiratory Syncytial Virus Infection

%%Children less than 1 year old:%%

\-bronchiolitis, pneumonia, fever, cough, dyspnea, cyanosis

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%%Children older than 1 year old:%%

\-febrile rhinitis and pharyngitis

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%%Older children and adults:%%

\-common cold

Rubella

\-remember this is a %%Togavirus NOT a Paramyxovirus%%

\-respiratory virus

\-different pathogenesis in children or adults than in fetuses

\-Symptoms (quite similar to measles except measles has Koplik’s spots)

* rash
* swollen lymph nodes
* malaise
* conjunctivitis
* coryza

Clinical Findings in %%Congenital%% Rubella Syndrome

\-Cataracts and other ocular defects (due to teratogenesis)

\-Heart defects

\-Deafness

\-Intrauterine growth retardation

* newborn has failure to thrive
* mortality within the first year

\-Microcephaly

* mental retardation

Measles, Mumps, Rubella Vaccine (MMR)

\-live attenuated virus

\-Measles: Schwartz or Moraten substrains of Edmonston B strain

\-Mumps: Jeryl Lynn strain

\-Rubella: RA/27-3 strain

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\-%%Vaccination schedule: one dose at 15 months, another dose between 4 and 6 years old or before junior high school%%

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\-%%Efficiency: 95% lifelong immunization with a single dose%%

@@Reoviruses@@

\-%%double-stranded RNA genome%%

\-%%naked, double-layered capsid%%

\*^^remember: reoviruses = “double, double”^^

\-%%segmented%%

\-resistant to environmental and gastrointestinal conditions

\-virus released by cell lysis

Double-Stranded RNA Viruses

\-genome serves as the template for mRNA transcription

\-virions carry the RNA dependent RNA polymerase in the core

\*Ex. reoviruses

Disease Mechanisms of Rotavirus

\-%%type of Reovirus%%

\-%%spread by fecal-oral route and possibly the respiratory route%%

\-cytolytic and toxin-like action on the intestinal epithelium causes loss of electrolytes and prevents reabsorption of water

\-%%disease can be very severe in infants younger than 24 months but asymptomatic in adults%%

\-large amounts of virus released during @@diarrheal phase@@

Rotavirus Clinical Symptoms

\*type of Reovirus

\-associated with gastroenteritis (usually self-limiting and usually complete recovery)

\-incubation period of 48 hr.

\-vomiting

\-diarrhea

\-fever

\-dehydration

\-may be fatal for malnourished and dehydrated infants in underdeveloped countries

Rotavirus Modes of Control

\*type of Reovirus

\-frequent handwashing

\-isolation of infected cases

\-vaccines available

* RotaTeq
* Rotarix

Calciviruses

\-%%linear, positive, single-stranded RNA genome%%

\-%%small, naked%%

\-name derived from 32 cup-shaped (calix, cup) surface depressions in the icosahedral capsid

\-%%includes Noroviruses, Astroviruses, and other small and round gastroenteritis viruses%%

Norovirus Pathogenesis

\*type of Calcivirus

\-%%responsible for about 90% of epidemic non-bacterial outbreaks of gastroenteritis in the world%%

\-%%transmitted by fecal-oral route in contaminated water and food%%

\-%%outbreaks commonly occur in closed or semi-closed communities such as cruise-ships, hospitals, and prisons%%

\-resistant to detergents, drying and acid; inactivated by chlorine-based disinfectants but less susceptible to alcohol or detergents

\-hand-washing = most effective way to eliminate spread of the virus

Rhabdoviruses

\-%%negative, single-stranded RNA virus%%

\-%%enveloped, non-segmented%%

\-%%bullet-shaped viruses%%

\-cell death and lysis occurs after infection with most of these viruses, %%except rabies which causes little cell damage%%

Rhabdoviruses: Rabies Virus Pathogenesis

\-rapidly progressive, incurable viral encephalitis

\-transmitted by bite of an infected rabid animal

\-resides in local area of infection for a long time before moving to CNS

\-once symptoms apparent, treatment is too late

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Infection of an Animal:

\-causes secretion of the virus in the animal’s saliva

\-promotes aggressive behavior (“mad dog”)

\-virus can be transmitted through:

* inhalation of aerosolized virus (found in bat caves)
* transplanted infected tissue (ex. cornea)
* inoculation through intact mucosal membranes

Filoviruses

\-negative, single-stranded RNA virus

\-enveloped, non-segmented

\
Ebola

\-endemic in Africa, discovered in 1976, Ebola river (Congo)

\-recurrent outbreaks of fatal human illness in Zaire and Sudan from 1970’s to 2000’s. 

\-West Africa epidemic 2014

\-5 subtypes (4 out of 5 occur in animal hosts native to Africa)

\-Clinical features similar to Marburg illness

\-Mortality: 50-90%, outbreak in Sudan (1976) had 53% fatality

\-Natural reservoir host of Ebola viruses remains unknown, but is likely animal-borne (bats)

\-Serological studies found low titer anti-Ebola antibody in healthy human populations in central Zaire and Sudan, suggesting that sub-clinical infections may occur

Filoviruses: Ebola

\-incubation time to clinical symptoms 2-21 days, most commonly 8-10 days

\-early symptoms are non-specific: fever, chills, muscle aches, malaise

\-spread from one person to another through direct contact with:

* Ebola-infected blood or body fluids
* objects, such as needles, that have been contaminated with infected body fluids

\-healthcare workers and others who come into close contact with infected patients (including corpses) have the highest risk of exposure

\-a patient must have symptoms to be infectious

Viruses vs. Prions

\-prions do not have/contain nucleic acids

\-prions do not have a defined morphology

\-prions are not disinfected by:

* formaldehyde
* proteases
* heat
* ionizing and UV radiation

\-prions have long incubation periods; for viruses the incubation period varies

\-prions aren’t targeted or eliminated effectively by immune responses or molecules

Prion Pathology

\-parts of the brain vacuolated or spongy

\-many cases also extensive deposits of extracellular protein fibrils or plaques

\-no signs of inflammation (no invasion of immune cells)

\
\
\-transmissible spongiform encephalopathies (TSE):

transmission of disease to experimental animal by intracranial injection of a homogenate of diseased tissue and subsequent serial passage to further animals

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\*slow brain infections

Retroviruses

\-two copies of positive-strand RNA genome (only diploid viruses)

\-enveloped spherical virion

\-reverse transcriptase carried in the virion

\-replicates through a DNA intermediate called a provirus

\-provirus integrates at random in host chromosome

Retroviruses: Human Oncoviruses

\-leukemia viruses that can cause cancer after a long latency period

\-include human T lymphotropic viruses

* HTLV-1
* HTLV-2
* HTLV-5

\-only HTLV-1 has been associated with disease

* Acute adult T cell lymphocytic leukemia (ATLL)
* HTLV-1-associated myelopathy (tropical spastic paraparesis) = non-oncogenic neurologic disease

@@How an Oncovirus Becomes Activated@@

\-by point mutation

\-by chromosomal rearrangement

\-by gene amplification

\-by retroviral activation

Human Immunodeficiency Virus (HIV)

\-Lentivirus

\-used to be termed lymphadenopathy virus (LAV) and HTLV-3

\-encodes several accessory genes

\-causative agent of the acquired immunodeficiency syndrome (AIDS)

\-AIDS = one of the most devastating epidemics ever recorded

HIV Transmission

\-inoculation in blood (ex. blood transfusion, needle sticks, tattoo needles)

\-sexual transmission

\-perinatal transmission (ex. intrauterine, peripartum, breast milk)

\-NOT transmitted by personal contact

Anti-HIV Drug Targets

\-%%Entry inhibitors:%% block attachment and/or fusion

\-%%Reverse transcriptase inhibitors:%% prevent conversion of RNA into DNA

\-%%Integrase inhibitors:%% prevent integration of provirus into host DNA

\-%%Protease inhibitors:%% prevent cell membrane from breaking to release viral particles

Parvoviruses

\-SMALLEST of the DNA viruses

\-%%single-stranded DNA genome%%

\-%%naked, icosahedral capsid%%

\-%%requirement of growing cells (B19) or helper virus (dependovirus) for replication%%

Parvoviruses that Infect Humans

\-%%Erythrovirus: B19 (fifth disease)%%

* Fifth of the childhood exanthemas: varicella, rubella, roseola, measles
* directly kills erythroid precursor cells
* RBC production stopped
* antibody production stops the viremia

\-%%Dependovirus:%% human “adeno-associated viruses” usually found in association with adenoviruses, which %%serve as “helpers” in their replication%%

\-%%Parvovirus:%% human bocavirus

Human Papillomaviruses

\-cause warts

\-at least 100 types

\-longer than polyoma

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\-%%double-stranded circular DNA genome replicated and assembled in the nucleus%%

\-%%small, icosahedral, naked virus%%

\-^^virus can cause lytic infections or oncogenic transformation (oncogenic potential)^^

Papillomavirus Modes of Control

\-%%Quadrivalent papillomavirus vaccine is available%% (GARDASIL, Merck) and contains human papillomavirus (HPV) types 6, 11, 16, and 18.



\-%%9-valent HPV is also available prepared from the purified virus-like particles of the major capsid protein of HPV%% types 6, 11, 16, 18, 31, 33, 45, 52 and 58.



\-%%recommended for girls and boys 9 to 11 years of age for the prevention of cervical cancer, precancerous or dysplastic lesions, and genital warts.%%

Human Polyomaviruses

\-BK virus = renal disease in immunocompromised patients

\-JC virus = progressive multifocal leuko-encephalopathy

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\-%%double-stranded circular DNA genome replicated and assembled in the nucleus%%

\-%%small, icosahedral, naked virus%%

\-^^virus can cause lytic infections or oncogenic transformation^^

DNA Virus: Adenovirus

\-%%dsDNA genome%%

\-%%naked capsid%%

\-medium sized

\-Diseases:

* %%respiratory infection, conjunctivitis, gastroenteritis, cystitis%%

\-Transmission:

* ^^respiratory^^
* ^^fecal-oral^^
* ^^close contact with infected patient (in conjunctivitis cases)^^

\-Diagnosis:

* by culture
* by viral antigen detection

\-Treatment

* %%none; in serious conjunctivitis cases steroids and antibiotics can be given%%

\-Prevention

* %%live enteric coated vaccine for military recruits%%

Poxviruses that Infect Humans

Orthopoxvirus:

* variola (major and minor)
* camelpox
* cowpox
* monkeypox
* vaccinia (small pox)

Molluscipoxvirus:

* molluscum contagiosum

Yatapoxvirus:

* Yaba monkey tumor virus tanapox (accidental infections)

Parapoxvirus:

* pseudocowpox, orf

Human Herpesviruses Classifications

\-alpha: herpes simplex virus 1 and 2 (HSV-1 and HSV-2), and varicella-zoster virus (VZV)

\-beta

\-gamma

Herpesviruses Common Biological Properties

\-%%Enzymology:%% encode enzymes for DNA metabolism, DNA synthesis, protein processing/modification

\-%%Nuclear replication:%% synthesis of DNA and capsid assembly occur in the nucleus of the infected cell

\-%%Cytolytic:%% Production of infectious progeny virus results in host cell death

\-%%Latency:%% All herpesviruses have the capacity for latency

Hepatitis A Virus

\-%%Picornavirus%%

\-%%positive, single-stranded RNA genome%%

\-%%”infectious, short-term” hepatitis%%

\-transmitted by fecal-oral route, high concentration in stool

\-mild disease

\-40% of acute hepatitis cases

\-contagious before symptoms appear

\-%%shellfish → filter feeders → concentrate virus%%

\-%%present in daycare centers%%

\-%%overcrowding has lead to more people being infected than actually realized%%

* %%Sweden: 13%%%
* %%USA: 44%%%
* %%Taiwan: 88%%%

Hepatitis B Virus

Treatment, Prevention, and Control:

\-Hepatitis B immune globulin within 1 week of exposure

\-Interferon-α for Chronic HBV

\-HIV reverse transcriptase inhibitor?

\-Blood screening

\-Lifestyle changes

\-Universal blood and body fluid precautions

Vaccination:

* Genetically engineered
* 95% effective