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Microbiology 3% exam weight

Virology — HIV, Hepatitis & Herpesviruses

Part of the NEET PG study roadmap. Microbiology topic microb-007 of Microbiology.

Virology — HIV, Hepatitis & Herpesviruses

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

HIV: Retrovirus (RNA); CD4+ T-cell count = disease progression marker. CD4 <200 = AIDS-defining illnesses.

Hepatitis key distinctions:

  • HAV: Fecal-oral, acute, self-limiting, no chronicity, IgM anti-HAV = acute infection
  • HBV: Blood/sexual, chronicity (10% adults), Hep B sAg (HBsAg) = infection; anti-HBs = immunity; HBcAb (anti-HBc) = exposure
  • HCV: Blood-borne, chronicity (80%), leading cause of cirrhosis and liver cancer; anti-HCV = screening; HCV RNA = active infection
  • Hepatitis B serology: HBsAg+ HBeAg+ anti-HBc IgM = acute/replicative phase; HBsAg- anti-HBs+ anti-HBc+ = recovered/immune

Herpesviruses (HHV 1–8): HSV-1 (oral), HSV-2 (genital), VZV (chickenpox/shingles), EBV (infectious mononucleosis), CMV (CMV retinitis in AIDS, congenital), HHV-6 (roseola), HHV-8 (Kaposi sarcoma)

Exam tip: HIV question → always check CD4 count and decide on OI prophylaxis. HBV question → read window period carefully.


🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

HIV / AIDS

Structure

  • Family: Retroviridae; genus Lentivirus
  • Genome: Two copies of +sense ssRNA; reverse transcriptase, integrase, protease
  • Envelope: gp120 (binds CD4 + coreceptor CCR5/CXCR4) and gp41 (fusion)
  • Target: CD4+ T helper cells (also macrophages, dendritic cells, microglia)

Transmission

Blood, sexual contact (receptive anal > receptive vaginal > insertive), perinatal (vertical), breastfeeding, needlestick (0.3% risk per exposure)

Clinical Stages

StageCD4 CountFeatures
Acute HIV infectionNormal or ↓Mononucleosis-like syndrome (fever, rash, lymphadenopathy, pharyngitis) 2–4 weeks after exposure
Chronic HIV infection (clinical latency)200–500Asymptomatic or persistent generalized lymphadenopathy
AIDS<200 cells/µLOIs, malignancies, wasting

AIDS-defining illnesses: PCP pneumonia, toxoplasmosis, Cryptococcal meningitis, disseminated MAC, esophageal candidiasis, CMV retinitis, Kaposi sarcoma, NHL, invasive cervical cancer, HIV encephalopathy, recurrent pneumonia, chronic cryptosporidiosis.

Opportunistic Infections by CD4 Count

CD4 CountInfection
<200PCP pneumonia, esophageal candidiasis, Kaposi sarcoma
<100Toxoplasma encephalitis, Cryptococcal meningitis
<50CMV retinitis, disseminated MAC, CNS lymphoma

Diagnosis

  • Screening: ELISA / CMIA (detects anti-HIV-1/2); window period 3–12 weeks
  • Confirmatory: Western blot (anti-HIV-1/2) or rapid point-of-care tests
  • Acute infection: HIV RNA PCR (viral load) — detectable within 7–14 days (before antibodies)
  • Monitoring: CD4 count (every 3–6 months), viral load (every 3–6 months)

HIV-1 vs HIV-2

  • HIV-1 is globally predominant; HIV-2 is West Africa (lower transmissibility, slower progression)
  • HIV-2 is inherently resistant to NNRTIs (efavirenz, nevirapine)

Treatment (HAART / cART)

Classes:

  • NRTIs (nucleoside reverse transcriptase inhibitors): Tenofovir (TDF/TAF), Emtricitabine, Zidovudine, Lamivudine
  • NNRTIs (non-nucleoside): Efavirenz, Nevirapine, Rilpivirine
  • Integrase inhibitors: Raltegravir, Dolutegravir, Bictegravir
  • Protease inhibitors: Atazanavir, Darunavir (ritonavir or cobicistat-boosted)
  • Entry inhibitors: Maraviroc (CCR5 antagonist), Enfuvirtide (fusion inhibitor)

Standard first-line: 2 NRTIs + 1 INSTI (e.g., TDF + FTC + Dolutegravir or Bictegravir/emtricitabine/TAF = Biktarvy)

Post-exposure prophylaxis (PEP): Start within 72 hours; continue for 28 days; 3-drug regimen (same as treatment)

PMTCT (prevention of mother-to-child transmission): Maternal HAART + neonatal zidovudine + avoid breastfeeding


Hepatitis Viruses

Comparative Overview

VirusTransmissionIncubationChronicityVaccine
HAVFecal-oral2–6 weeksNo (always self-limiting)Yes (HepA)
HBVBlood, sexual, perinatal6 weeks–6 months10% adultsYes (HepB)
HCVBlood6–12 weeks80%No
HEVFecal-oral2–8 weeksRare (pregnant women at risk)No

Hepatitis B — Serology

MarkerSignificance
HBsAgActive infection (acute or chronic); first marker to appear
Anti-HBs (HBsAb)Immunity (natural recovery or post-vaccine)
Anti-HBc (HBcAb)Exposure to HBV (does NOT indicate immunity)
HBeAgActive viral replication; high infectivity
Anti-HBe (HBeAb)Low infectivity; disease resolution
HBV DNAActive replication; quantitative

Window period: HBsAg has cleared but anti-HBs hasn’t appeared; only HBcAb IgM/IgG is positive → this period has highest infectivity

HBV and Liver Cancer

  • HBV is a direct oncogenic virus (like HPV for cervical cancer)
  • Chronic HBV → cirrhosis → hepatocellular carcinoma (HCC)
  • HBV X protein (HBx) is oncogenic
  • HCC surveillance: 6-monthly AFP + liver ultrasound in cirrhotics and chronic HBV carriers

Hepatitis C

  • Leading cause of liver transplantation in the US
  • Leading cause of chronic liver disease, cirrhosis, and HCC worldwide
  • Genotypes 1 (most common globally), 2, 3; genotype determines treatment duration
  • Treatment: Direct-acting antivirals (DAAs) — Sofosbuvir/Ledipasvir, Elbasvir/Grazoprevir, Glecaprevir/Pibrentasvir; cure rates >95%

Herpesviruses

HSV-1 and HSV-2

  • Family: Herpesviridae (HHV-1 and HHV-2); large dsDNA virus
  • Transmission: HSV-1 — oral contact (kissing, shared utensils); HSV-2 — sexual contact
  • Primary infection: Often asymptomatic; can cause gingivostomatitis (HSV-1) or genital herpes (HSV-2)
  • Latency: Neuronal ganglia (HSV-1 → trigeminal ganglion; HSV-2 → sacral ganglia)
  • Reactivation: Fever, stress, immunosuppression → cold sores (HSV-1) or genital ulcers (HSV-2)
  • Diagnosis: Tzanck smear (multinucleated giant cells), PCR, viral culture
  • Treatment: Acyclovir, Valacyclovir, Famciclovir (DNA polymerase inhibitors)

Varicella-Zoster Virus (VZV, HHV-3)

  • Primary infection: Chickenpox (varicella) — vesicular rash “dew drops on rose petal,” centripetal distribution, crops at different stages
  • Complications: Pneumonia (adults), encephalitis, cerebellar ataxia, neonatal varicella (if mother infected 5 days before to 2 days after delivery)
  • Reactivation: Herpes zoster (shingles) — dermatomal, vesicular rash; most common in thoracic dermatomes; postherpetic neuralgia (persistent pain after rash heals) is major complication
  • Vaccine: Varicella vaccine (live attenuated) for children; shingles vaccine (RZV/Shingrix) for adults >50 years (recombinant, not live)

Epstein-Barr Virus (EBV, HHV-4)

  • Infectious mononucleosis: “Kissing disease”; fever, pharyngitis (exudative tonsillitis), posterior cervical and axillary lymphadenopathy, splenomegaly, fatigue
  • Hallmark: Atypical lymphocytosis (Downey cells = CD8+ T cells); heterophile antibodies (Monospot test) — positive in 85% of adolescents/adults
  • EBV associations: Burkitt lymphoma (African jaw, associated with EBV + malaria co-infection), nasopharyngeal carcinoma (China/Southeast Asia), Hodgkin lymphoma (some cases), post-transplant lymphoproliferative disorder, oral hairy leukoplakia (HIV/AIDS)
  • Diagnosis: Heterophile antibody test (Monospot), anti-VCA IgM/IgG, EBNA IgG

Cytomegalovirus (CMV, HHV-5)

  • Prevalence: 50–80% adults seropositive
  • Congenital CMV: #1 non-genetic cause of sensorineural hearing loss; petechial rash (“blueberry muffin”), periventricular calcifications, microcephaly, hepatosplenomegaly
  • CMV in immunocompromised: Retinitis (most common in AIDS, CD4 <50; “pizza pie” or “cottage cheese and ketchup” fundoscopic appearance), colitis, pneumonitis
  • Infectious mononucleosis-like syndrome in immunocompetent individuals
  • Diagnosis: Shell vial culture (early antigen), PCR, CMV antigenemia; heterophile-negative mononucleosis
  • Treatment: Ganciclovir (first-line for CMV retinitis), Valganciclovir (oral prodrug)

🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

HIV — OI Prophylaxis Thresholds

OIProphylaxis TriggerDrug
PCP pneumoniaCD4 <200 or oropharyngeal candidiasisTMP-SMX
ToxoplasmosisCD4 <100 + positive Toxoplasma IgGTMP-SMX
Disseminated MACCD4 <50Azithromycin
Cryptococcal meningitisNot routinely recommended; treat when diagnosedAmphotericin B + Flucytosine
TBPositive IGRA or exposureIsoniazid + pyridoxine

Immune Reconstitution Inflammatory Syndrome (IRIS)

  • Occurs within weeks–months of starting HAART
  • Paradoxical worsening of OI symptoms as immune system recovers
  • More common when starting HAART at very low CD4 counts
  • Treatment: Continue HAART; short course of corticosteroids for severe cases
  • Common unmasking IRIS: CMV retinitis, TB, MAC, PML

Prion Diseases (NEET PG Note)

Not viral but often asked together: Prion diseases are rapidly progressive dementias with spongiform pathology. Creutzfeldt-Jakob disease (CJD) is the most common. Kuru in Fore tribe of Papua New Guinea (ritual cannibalism). Rapidly progressive dementia with startle myoclonus, ataxia. EEG: periodic sharp wave complexes. 4-1-4-1 pattern. No known treatment.

Key NEET PG Pearls

  1. HIV: CD4 <200 = PCP prophylaxis (TMP-SMX); CD4 <100 = Toxoplasma prophylaxis; CD4 <50 = MAC prophylaxis (azithromycin)
  2. AIDS malignancies: Kaposi sarcoma (HHV-8), NHL (EBV), cervical cancer (HPV)
  3. Oral hairy leukoplakia on lateral tongue = EBV in HIV (not candidiasis, doesn’t scrape off)
  4. Hepatitis B: HBsAg positive = infection; anti-HBs positive = immunity; anti-HBc alone = window period or occult infection
  5. Hepatitis C is the leading cause of chronic liver disease, cirrhosis, and HCC; treat with DAAs
  6. Hepatitis A: IgM anti-HAV = acute infection; IgG anti-HAV = past infection or vaccine; never becomes chronic
  7. EBV infectious mononucleosis: Fever + exudative tonsillitis + posterior lymphadenopathy + splenomegaly + atypical lymphocytes; Monospot positive
  8. VZV reactivation (shingles): vesicular rash in dermatomal distribution; treat within 72 hours with valacyclovir
  9. Congenital CMV: Most common congenital infection; sensorineural hearing loss is most common sequela
  10. CMV retinitis in AIDS: “pizza pie” or “cottage cheese and ketchup” appearance; treat with ganciclovir/valganciclovir

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