Microbiology — HIV and Viral Hepatitis, NMC MBBS licence examination syllabus (Nepal Medical Council).
HIV and viral hepatitis: chronic infections with long silences
Both are diseases where the damage is done quietly, years before anyone feels ill.
HIV and the blood-borne hepatitides share a shape that makes them unusual among infections. They do not announce themselves. A person can carry either for a decade in good health while the immune system or the liver is steadily damaged, and by the time symptoms arrive, much of the harm is established. This is why both are found by testing people who feel well rather than by waiting for a presentation.
It also explains why the clinical reasoning in this chapter is mostly about interpretation — what a CD4 count predicts, what a negative test does and does not exclude, and what a set of hepatitis B markers is telling you about a patient who has no symptoms at all.
🩺 Where this lives: Both infections are surrounded by stigma, and stigma is a clinical problem, not a social footnote. Fear of disclosure delays testing, delays presentation and interrupts treatment — and interrupted antiretroviral therapy is precisely what produces resistance. Confidentiality, informed consent and a non-judgemental manner are therefore part of the medicine here, in the same way that a correct drug choice is. A patient who does not trust the service does not return to it.
💡 A note on numbers. This chapter gives no drug regimens and no doses. Antiretroviral and hepatitis therapy change with national guidelines and resistance patterns, and first-line combinations in Nepal are set by the national programme. CD4 bands are given as higher, low and very low rather than as figures, because published thresholds differ — learn what the count predicts, and take the numbers from your current national guideline.
What HIV does
Everything clinical about HIV follows from one fact: the virus infects the CD4 T-helper cell, which coordinates cell-mediated immunity. That is the arm of the immune system that handles organisms living inside cells — viruses, fungi, mycobacteria, protozoa. So as CD4 cells are depleted, defence fails against those organisms in a roughly predictable sequence, which is why the CD4 count is not merely a number but a prediction of which illness to expect.
TWO TESTS THAT ANSWER DIFFERENT QUESTIONS
CD4 COUNT — how much immunity is LEFT.
Predicts which opportunistic infections are
a risk, and therefore what prophylaxis is
needed. It is a measure of DAMAGE DONE.
VIRAL LOAD — how much virus is PRESENT.
Measures how well treatment is working and
how infectious the person is. It is a
measure of DISEASE ACTIVITY.
On effective treatment the viral load falls first, and the
CD4 count recovers afterwards — often slowly, and often
incompletely if treatment started late. That lag is the
single best argument for early diagnosis.
TUBERCULOSIS deserves separate mention: unlike most
opportunistic infections, it occurs at ANY CD4 count, and
it is the commonest serious infection in people with HIV
in many high-burden settings. HIV and TB must always be
thought about together — test for HIV in TB, and screen
for TB in HIV.
Testing
💡 Exam angle: the window period is asked constantly and matters clinically. Between infection and a detectable test result, a person is infected and infectious but tests negative — so a single negative test shortly after a high-risk exposure does not exclude infection and must be repeated. The other classic question is the infant under 18 months: maternal antibody crosses the placenta, so an antibody test may be positive in an uninfected baby. Diagnosis in that age group requires virological testing.
Treatment and prevention
Two principles carry most of the marks. First, combination therapy — several drugs together, because HIV mutates fast enough that single-agent treatment selects resistance quickly. Second, treatment is prevention: a person on effective therapy with a sustained undetectable viral load does not transmit HIV sexually. That finding reshaped public health policy, and it is also the most useful thing you can tell a newly diagnosed patient who is frightened for their partner.
Viral hepatitis
THE ORGANISING RULE
ROUTE OF TRANSMISSION PREDICTS CHRONICITY.
FAECAL-ORAL (A, E) → acute illness, no chronic carriage
BLOOD-BORNE (B, C, D) → can persist for life
And chronic infection is what causes CIRRHOSIS and
HEPATOCELLULAR CARCINOMA. So the viruses that matter for
long-term liver disease are the blood-borne ones.
THREE EXCEPTIONS AND ODDITIES WORTH KNOWING:
HEPATITIS E IN PREGNANCY — usually a self-limiting illness,
but it carries a substantially higher risk of severe and
fulminant disease in pregnant women. This is a
well-recognised and heavily examined exception.
HEPATITIS B IN INFANCY — the YOUNGER the age at infection,
the HIGHER the chance of chronic carriage. Infection at
birth very often becomes chronic; infection in adulthood
usually resolves. This is why birth-dose vaccination and
prevention of mother-to-child transmission matter so much.
HEPATITIS D — cannot replicate without hepatitis B. It only
infects people who already carry B, and it makes the
disease worse. Vaccinating against B therefore prevents D.
HEPATITIS C is often silent for years and is now CURABLE
with direct-acting antiviral therapy — which makes finding
it worthwhile in a way that was not true a decade ago.
Reading hepatitis B serology
💡 Exam angle: nearly every hepatitis B serology question turns on anti-HBc. Vaccination produces antibody to the surface antigen only — so a vaccinated person is anti-HBs positive and anti-HBc negative. Someone who cleared a real infection has met the whole virus, so they are anti-HBs positive and anti-HBc positive. If you learn one thing from this section, learn that: core antibody means the virus itself was there.
Clinical reasoning: four presentations
🔍 Case 1 — a negative test that reassures nobody
PresentationA man attends 10 days after a high-risk exposure, anxious. An HIV test is negative and he is told he is in the clear.
TrapTreating a single early negative test as conclusive.
ReasoningThis is within the window period, when an infected person is both infectious and test-negative. A negative result here excludes nothing.
AnswerExplain the window period, arrange repeat testing per the national algorithm, discuss risk reduction, and assess whether post-exposure prophylaxis is indicated — that decision is time-critical and follows local protocol.
🔍 Case 2 — breathless with a normal-sounding chest
PresentationA man with untreated HIV and a very low CD4 count has weeks of dry cough and worsening breathlessness on exertion. Auscultation is relatively unremarkable and he desaturates on walking.
Key cluesSubacute course, dry cough, marked exertional desaturation, few chest signs, very low CD4.
ReasoningThis pattern suggests Pneumocystis pneumonia, an opportunistic infection of advanced immunosuppression. But TB occurs at any CD4 count and is common in high-burden settings, so it must be actively excluded rather than assumed away.
AnswerUrgent assessment with oxygenation measured on exertion, investigate for both Pneumocystis and TB, and treat per national guideline. Start antiretroviral therapy with specialist input, and address prophylaxis.
🔍 Case 3 — the serology that looks confusing
PresentationA healthy applicant for a health-worker post has: HBsAg negative, anti-HBs positive, anti-HBc negative. She is told she has had hepatitis B in the past.
Key markeranti-HBc is negative.
ReasoningCore antibody appears only after infection with the actual virus; vaccination cannot produce it. Surface antibody without core antibody is the signature of successful vaccination, not past infection.
AnswerShe is vaccinated and immune, with no evidence of previous infection. Reassure and correct the record — this distinction matters for her occupational health file.
🔍 Case 4 — jaundice in pregnancy
PresentationA woman in the third trimester develops jaundice, nausea and malaise during a community outbreak of hepatitis linked to contaminated water. She is managed as a routine self-limiting illness.
The concernHepatitis E in pregnancy.
ReasoningHepatitis E is usually mild and self-limiting, but in pregnancy — particularly later pregnancy — it carries a substantially higher risk of severe and fulminant hepatic failure. Routine outpatient management underestimates that risk.
AnswerTreat as high risk: careful monitoring for signs of liver failure and encephalopathy, obstetric and hepatology involvement, and admission per local protocol. Public health measures address the water source for the wider outbreak.
Commonly confused
Confusion
The distinction
Why it matters
CD4 count vs viral load
Damage done versus disease activity
They answer different clinical questions.
Negative test vs not infected
The window period
Early negative tests must be repeated.
Antibody vs virological testing in infants
Maternal antibody crosses the placenta
Under 18 months needs virological testing.
Opportunistic infections vs TB
TB occurs at any CD4 count
Never exclude TB because the count is preserved.
anti-HBs alone vs with anti-HBc
Vaccination versus past infection
Core antibody means the real virus was met.
Faecal-oral vs blood-borne hepatitis
Only blood-borne viruses persist
Chronicity drives cirrhosis and liver cancer.
Hepatitis E generally vs in pregnancy
Much higher risk of severe disease in pregnancy
Changes the level of monitoring required.
Adult vs infant hepatitis B
Younger infection means higher chronicity
Justifies birth-dose vaccination.
Rapid revision
MUST-KNOW FACTS
1. HIV infects the CD4 T-HELPER cell.
2. Loss of CD4 cells impairs CELL-MEDIATED immunity.
3. The CD4 count predicts WHICH infections occur.
4. Viral load measures virus; CD4 measures remaining immunity.
5. On treatment, viral load falls first; CD4 recovers later and slowly.
6. TUBERCULOSIS occurs at ANY CD4 count.
7. Test for HIV in TB, and screen for TB in HIV.
8. Pneumocystis: subacute dry cough, exertional desaturation, few signs.
9. The WINDOW PERIOD — infectious, infected, and test-negative.
10. A single early negative test does not exclude HIV; repeat it.
11. Infants under 18 months need VIROLOGICAL testing, not antibody.
12. Maternal antibody crosses the placenta and confuses infant serology.
13. HIV testing needs informed consent and counselling.
14. Stigma delays testing and interrupts treatment — it is a clinical problem.
15. Treat with COMBINATION therapy — monotherapy selects resistance.
16. Treatment is recommended for everyone diagnosed, at any CD4 count.
17. ADHERENCE determines whether treatment works.
18. Sustained undetectable viral load = NOT sexually transmitted.
19. Prevention of mother-to-child transmission: testing, maternal ART, infant prophylaxis.
20. PEP after exposure is time-critical; PrEP prevents acquisition.
21. Hepatitis A and E are FAECAL-ORAL and do not become chronic.
22. Hepatitis B, C and D are BLOOD-BORNE and can persist.
23. Chronic hepatitis causes CIRRHOSIS and HEPATOCELLULAR CARCINOMA.
24. HEPATITIS E IS SEVERE IN PREGNANCY.
25. Hepatitis B acquired in INFANCY very often becomes chronic.
26. Hepatitis D needs hepatitis B to replicate.
27. Vaccinating against B also prevents D.
28. Hepatitis C is often silent — and is CURABLE with antivirals.
29. HBsAg positive = currently infected.
30. anti-HBs positive = immune (vaccine or resolved infection).
31. anti-HBc positive = has met the actual VIRUS — never from vaccine.
32. VACCINATED: anti-HBs positive, anti-HBc NEGATIVE.
33. PAST INFECTION: anti-HBs positive AND anti-HBc positive.
34. HBeAg indicates high replication and high infectivity.
💡 Exam angle: three threads recur — what the CD4 count predicts (and that TB ignores it), what a negative HIV test fails to exclude, and the anti-HBc distinction between vaccination and past infection. Each is a single idea that answers a whole family of questions, which makes them unusually good value for revision time.
Syllabus points
Why HIV targets the CD4 cell
How the CD4 count predicts the illness
CD4 count versus viral load
Tuberculosis occurs at any CD4 count
The window period and repeat testing
Testing infants under 18 months
Combination therapy and adherence
Treatment as prevention
Preventing mother-to-child transmission
Route of transmission predicts chronicity
Hepatitis E in pregnancy
Why infant hepatitis B becomes chronic
Reading hepatitis B serology
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