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recap
Herpesviridae = family of DNA viruses cause disease in human/animal
8 human herpesviruses (HHV-1 to HHV-8)
HHV-1 (HSV-1): oral herpes (cold sores)
HHV-2 (HSV-2): genital herpes
HHV-3 (VZV): chickenpox & shingles
HHV-4 (EBV): infectious mononucleosis, Burkitt’s lymphoma, nasopharyngeal carcinoma
HHV-5 (CMV): mononucleosis-like illness, retinitis (immunocompromised) HHV-6: roseola (sixth disease)
HHV-7: roseola-like illness
HHV-8 (KSHV): Kaposi’s sarcoma
rhadinovirus = KSHV = Kaposi's sarcoma herpesvirus (not be confused with Kaposi's varicelliform eruption
Human Herpesvirus 3 (HHV-3) = Varicella-Zoster Virus
cause varicella (chickenpox) & herpes zoster (shingles)
2 diff disease due to identical organism
chicken pox = primary infection
herpes zoster = reactivation of illness
Varicella (Chickenpox)
cause = VZV
transmit = enter via mucosa of upper resp tract (high infect) > viremia > spread to skin > replic in epith cells > vesicular rash
incubation = 2 weeks
clinical finding = malaise, fever, diffuse vesicular rash (oral mucosa too)
treatment = self limiting, symptomatic management
Varicella-Zoster Infects
cause = reactivation of VZV
pathogenesis = latent in dorsal root / cranial nerve ganglia
triggers = immunosuppresion, trauma, drug, malignancy
clinical = malaise, fever, severe localized pain, vesicular rash along a nerve (dermatomal distrib / dermatome
- roses from hell vasicular rash
treatment = analgesic (for pain), antiviral (acyclovir), vaccine (for prim infect + reactive)


HHV-4 = Epstein-Barr Virus
etiology = Epbar virus (EBV) (HHV-4)
target tissue = lymph nodes & spleen (incs lymphocytes aka B cells)
^establishes lifelong latency w potential reactivate
assoc diseases
infectious mononucleosis (kissing disease)
burkitt lymphoma & other B-cell lymphomas
nasopharyngeal carcinoma
oral hairy leukoplakia
post-transplant lymphoproliferative disorders
transmission/patho = via saliva (kissing disease or shared drink)
incubation = 4-7 week
clinical = fever, sorethroat, enlarged tender nodes, fatigue, mild jaundice, gingival bleed
disease characs
acute infect of lymphoid tissue
most common adolescent (15-20)
self limiting (fatique)
HHV-5 = Cytomegalovirus (CMV)
etiology = CMV (herpesvirus fam, HHV-5)
congenital infection (intrauterine/perinatal)
usually asymptomatic in healthy ppl
high risk = neonates (newborn) can be deaf & intellectual disability later
immunocomps = transplant receipient, leukemia ppl, HIV/AIDs ppl
CMV is a AIDs-defining infection
transmit = body fluids
incubation = 4-8 week
clinical
infants = severe disease (CNS damage, jaundice, pneumonitis, dev delay)
adults = mononucleosis-like illness
RETINITIS
latency + reactivation = high prevalence
no proven regimens for therapy and prevention of CMV infect
treatment for EBV & CMV
EBV (infectious mononucleosis)
support care (rest hydrate)
no specif antiviral therapy
steroids (only in severe)
SUPPORTIVE CARE
CMV - antivirals for high-risk patients
Ganciclovir / Valganciclovir
used in immunocomps or severe disease
supportive care in mild cases
MAY REQ ANTIVIRALS IN HIGH RISK PATIENT
Which virus causes chickenpox?
A. Herpes simplex virus
B. Varicella-zoster virus
C. Epstein–Barr virus
D. Cytomegalovirus
Which route is the most common mode of transmission for chickenpox?
A. Fecal–oral transmission
B. Vector-borne transmission
C. Respiratory droplets and direct contact
D. Contaminated food
Which statement regarding varicella-zoster virus is CORRECT?
A. It is an RNA virus
B. It remains latent in salivary glands
C. It can reactivate later in life as shingles
D. It is transmitted primarily through blood transfusion
A university student presents with fever, fatigue, sore throat, and cervical lymphadenopathy. Which virus is the most likely cause?
A. Varicella-zoster virus
B. Cytomegalovirus
C. Epstein–Barr virus
D. Herpes simplex virus type 1
A patient with advanced HIV infection develops retinitis caused by a herpesvirus. Which virus is the most likely cause?
A. Epstein–Barr virus
B. Varicella-zoster virus
C. Cytomegalovirus
D. Herpes simplex virus type 1
Congenital CMV infection is clinically important because it may cause:
A. Dental caries only
B. Hearing loss and developmental abnormalities
C. Appendicitis
D. Hyperthyroidism

Papillomavirus - warts
etiology = HPV
patho = infect epithelial cells of skin & mucous mems
clinical
cutaneous warts (common, plantar, flat)
genital wart
laryngeal wart
oral finding
papular or nodular lesion
surface = papillary *cauliflower like* projections
transmit = direct contact
treatment = excision (surg remove) or chemical remove (trichloracetic acid)
know theres many types w different conditions
range from benign proliferative lesions > oncogenic disease
depend on strain & loc
HPV vax = Gardasil
only for 6, 11, 16, 18
16/18 = high risk type assoc w oropharyngeal cancer
6/11 = low risk type (90% genital warts)
HPV infect cause nearly all cervical cancers


Hepatitis
inflam disease of liver caused by variety of virus (transmit dep on type)
acquire thru blood, body fluid, food/water, too much alc (non-infectious cause)
common symptom = malaise, jaundice, dark pee, pale fatty stool
at least 6 strains of hep viruses (A-G)
if see “non-hep” = less common form that dont fit classifs
Hep A
eti = small non-envelope single-strand RNA virus (picornavirus)
transmit = prim fecal-oral route (contam food/water)
mostly children
infectious before symptoms appear
virus present in feces + saliva
no chronic infect/carrier state
symptoms
fever, nausea, abd discomfort, jaundice (common in adult)
resemble influ-like illness
self limiting (goes away on own)
diagnosis
IgM anti-HAV (hep A virus) → early/acute infect
IgG anti-HAV → later in disease/immunity
outcome + prevent
lifelong immunity after infect
no chronic disease or carrier state
combined hep A+B vaccine (initial then booster)
low risk for dentistry bc fecal-oral route
Hep B
eti = enveloped double-stranded DNA virus (hepadnavirus)
target = infect lymphocyte → liver inflam
many transmit = body fluid, needle share, sex, mother-child
dental relevance = blood contam saliva
clinical
many infect initially asymptomatic
fatigue nausea abd pain jaundice
carrier state
most recover completely, little develop chronic carrier state
chronic lead to → cirrhosis, hepatocellular carcinoma (liver cancer)
remain infect for yrs for chronic
diagnosis = blood testing
serological markers determ > active infect, immunity, infectivity, carrier state
important markers
HBsAg – Indicates current infection/carrier state
anti-HBs – Indicates recovery or immunity after vaccination
HBeAg – Indicates high infectivity
anti-HBc – Indicates previous or ongoing infection
prevent = hep B vax
recombinant vax (use DNA techno in yeast cells, not live)
engerixB, recombivax
treatment = antiviral therapy (for chronic)
occupational risk = dental bc blood bourne


Hep C
eti = hep C virus (HCV) enveloped single stranded RNA virus (flavivirus)
formerly non-A, non-B hepatitis
primarily blood borne
exist as 6 genotypes
viral rna remain intact up to 7 days room temp
transmit
injection/drug use, blood stuff, needle, org transplant, sex, mom-kid
clinical
often asymptomatic
symptoms. fatigue nausea abd discomf (SIMILAR TO B)
chronic infect
80% develop this, can persist for decades
lead to cirrhosis, chronic liver disease, hepatocellular carcinoma
diagnose
serological blood testing (ELISA)
PCR testing for detect early infect
treat
not always required
direct acting antivirals (DAA)
high cure rate
prev
no vax available
dent/oral manifestation
greatest risk is needle-stick injury
oral lichen planus
salivary gland disease
inc risk oral malignancy
What is the primary route of transmission for Hepatitis A?
A. Blood transfusion
B. Sexual contact
C. Fecal–oral route
D. Needle-stick injuries
Hepatitis B is primarily transmitted through:
A. Airborne droplets
B. Blood and body fluids
C. Insect bites
D. Contaminated food only
A patient who carries Hepatitis B virus without symptoms is referred to as:
A. Immunocompromised
B. Opportunistic
C. A carrier
D. Seronegative
Which statement about Hepatitis A is CORRECT?
A. It commonly causes chronic liver disease
B. It is usually self-limiting
C. It requires integration into host DNA
D. It is primarily blood-borne
Which preventive measure is MOST effective against Hepatitis A?
A. Antibiotics
B. Antifungal therapy
C. Vaccination and good hygiene
D. Corticosteroids
Which route is MOST associated with Hepatitis C transmission?
A. Fecal–oral route
B. Respiratory droplets
C. Blood exposure
D. Contaminated water
Hep D - Delta Hepatitis
eti = HDV hepatitis d virus (defective single-strand RNA envelope from HBV)
requires ACTIVE HBV INFECT to survive & replic
^borrows its outer viral envelope from its surface antigen
HDV inc severity of HBV (CO-INFECTION/SUPERINFECTION)
transmit = blood, needle, sex, perinatal
epidemiology = common in inject drug user, africa, amazon, middle east
clinical
often asymptomatic
freq cause jaundice
severe acute hepatitis
fulminant liver disease
chronic infect -→ cirrhosis (late stage liver infect)
diagnose = detect of delta antigen/antibody (ELISA)
treat = limited resp to interferon therapy
prev = hep B vax
Hep E
eti = hep E virus (HEV) single stranded RNA virus
similar to Hep A
self limiting, no chronic
transmit = fecal-oral route thru water
areas of poor sanitation
epidemiology
large outbreak/epidemic may occur
adolescent/young adult
intrafamilial/parental spread rare
high risk = pregnant (esp 3rd trimester) → inc mortality
diagnosis = ELISA, PCR, Western blot
dental = minimal bc fecal oral not blood
Hep G - Human Pegivirus (HphV-1)
eti = RNA virus related to Hep C virus (family Flaviviridae)
transmit = blood
common in injection drug user / blood recepient
little/no symptom, clinically unclear
overall dental implics
real risk of viral infect in dental setting
HCV transmit prim assoc w exposure to blood & needlestick

HIV = human immunodeficiency virus
eti = HIV virus enveloped single stranded RNA (retroviridae)
involve destruct of immune sys, infect CD4 + T lympocytes (helper t-cells reg immune resps)
make ppl suscept to life threatening infect/disease
contains
reverse transcriptase enzyme
viral RNA genome
2 major types
HIV-1 = (common worldwide)
HIV-2 = (less transmissible, mainly africa)
without treatment HIV progress to AIDS in 2-12 yrs
transmit
sex (most common)
blood, needle, preg/birth/breastfeed
not rlly saliva
STEPS OF INFECT
HIV selectively attach to T4 lymphocytes (helper)
viral RNA quickly converted → viral DNA (via reverse transcriptase)
viral DNA integ > host cell DNA
permanent infect of lymphocyte & future cells
can be latent for years then start prod new virus particles
virus prod continue to destroy
3-4 week after infect…symptoms (PHOTO)
diagnosis
antibodies (to recog) dev 6-12week after infect
window period before detectable
screening in 2 assays
HIV antigen/antibody test
ELISA (must retest bc of false negs)
then confirmatory testing
western blot/sipplemental immunoassays
PCR testing
detect viral RNA &. measure viral load
treatment
no cure/vaccine
treatment symptomatic
combination of antiretroviral therapy (ART supress viral replication & preserve immune fxn)

AIDS (acquired immunodeficiency syndrome)
advanced HIV infect stage
as HIV replic/destroy T4, immune sys weakens
diagnose when CD4+ count less than 200 cells/µL OR AIDs-defining illness develops
opportunistic infects & malignancies become common
ex: pneumocytis jirovecii pneumonia (PCP is lung infect in immunocomps)
kaposi sarcoma (cancer lining lymph & vessles make masses)
tuberculosis
toxoplasmosis
oral manifestation
candidiasis - thrush seen in 85% cases
distinct mouth odor
hairy leukoplakia (lat borders of tongue)
herpes typ1
angular chelitis
NUG
kaposi sarcoma (vascular lesion in oral)
HHV-7 & HHV-8 (Kaposi Sarcoma-Assoc Herpesvirus)
HHV-7
T-lymphotrophic virus
assoc w rash illness (roseola-like)
HHV-8 (Kaposi Sarcoma Virus)
cause kaposi
vascular tumor seen in HIV/AIDs & immunocomps
these establish latwncy
HHV6 & HHV7 very common (70-90%)
KEY TAKEAWAYS
these viruses are common
establish latency
HHV 8 strong link to malignancy (cancer)

Risk of HIV transmit in HealthCare***
risk of HIV transmit after single needlestick = 0.3%
lower than HCV (3-10%)
much lower than HBV (up to 30%) MOST*
VIEW REVIEW PHOTO ***
review
HIV primarily targets which cells of the immune system?
A. Red blood cells
B. Neutrophils
C. CD4+ T lymphocytes
D. Platelets
Which enzyme allows HIV to convert its RNA into DNA?
A. Integrase
B. Reverse transcriptase
C. Protease
D. DNA ligase
Which route is the MOST common mode of HIV transmission worldwide?
A. Saliva
B. Sexual contact
C. Airborne droplets
D. Food contamination
A patient is diagnosed with AIDS when:
A. HIV antibodies are first detected
B. The viral load reaches zero
C. CD4+ count falls below 200 cells/µL or an AIDS-defining illness develops
D. Oral candidiasis is present
A dental hygienist experiences a needle-stick injury involving blood from a patient with untreated HIV infection. What is the approximate risk of HIV transmission after a single occupational needle-stick exposure?
A. 0.03%
B. 0.3%
C. 3%
D. 30%

Post-Exposure Prophylaxis (PEP) testable
should begin soon as possible (within 2 hr)
uses combination antiretroviral therapy (ART)
goal
reduce risk of HIV infect after occupational expose
early treat signif lower risk of seroconversion(body start producing antibodies in resp to infect)
Needlestick/sharp exposure protocol
1. Stop and attend to the injury immediately
Allow the wound to bleed gently; do not squeeze or scrub
Wash with soap and water; flush mucous membranes or eyes with water or saline
Do not apply caustic agents
Report
Notify the supervising dentist / employer at once and record the incident
Assess the exposure and the source
Type of injury, device, depth, volume of blood, source patient status
Seek the source patient’s consent for HBV, HCV and HIV testing
Seek medical assessment the same day
Baseline serology for the exposed worker (HBV, HCV, HIV)
Check the worker’s hepatitis B immunization and anti-HBs status
Post-exposure prophylaxis (time-critical)
HIV: combination ART, ideally within 2 hours see PEP slide
HBV: HBIG and/or vaccine if not immune
HCV: no prophylaxis — monitor and treat early if seroconversion occurs 6. Follow-up serology and counselling as directed (typically to 6 months)
