AIDS — HIV Infection

NCERT grounding

NCERT Class XII Biology Chapter 7, Section 7.3, opens by spelling out the acronym and the etiology in two sentences that every NEET aspirant must internalise verbatim. The textbook then sets the disease in historical context — first reported in 1981, more than 25 million deaths over the next quarter century — and pivots to the four exclusive routes of HIV transmission, the macrophage-to-TH-cell pathogenesis, ELISA as the diagnostic mainstay and prevention as the only durable strategy. NIOS Senior Secondary Biology, Lesson 29 (Some Common Human Diseases), classifies HIV among the viral communicable diseases and reinforces the same transmission inventory.

“AIDS stands for Acquired Immuno-Deficiency Syndrome. This means deficiency of immune system, acquired during the lifetime of an individual indicating that it is not a congenital disease.”

NCERT Class XII · Section 7.3

The phrase NCERT uses — “acquired during the lifetime” — is the wedge that distinguishes AIDS from inherited immunodeficiencies such as SCID. The same paragraph also clarifies that ‘syndrome’ denotes a cluster of symptoms rather than a single sign, an idea NEET has tested through statement-pair questions on what AIDS is and is not.

HIV biology, pathogenesis and control

The virus: a retrovirus with two RNA copies

HIV belongs to the family Retroviridae, genus Lentivirus. Each virion is roughly spherical, 100–120 nm across, and is bounded by a lipid envelope studded with the glycoprotein spikes gp120 and gp41. Internal to the envelope sits a conical capsid built from the p24 protein. The capsid carries two identical single-stranded positive-sense RNA molecules — the diploid genome that distinguishes retroviruses — packaged with three viral enzymes: reverse transcriptase, integrase and protease. NCERT highlights the envelope-plus-RNA architecture in Figure 7.6.

The label ‘retrovirus’ refers to reverse flow of genetic information. Where the central dogma reads DNA → RNA → protein, retroviruses force the cell to copy RNA back into DNA before the standard arc resumes. That single inversion is the molecular hinge of AIDS pathogenesis, the drug target of AZT and the reason HIV integrates permanently into host chromosomes.

Routes of transmission — the canonical four

NCERT pares HIV transmission down to four exclusive routes. Every other claim — handshakes, sharing food, mosquito bites, swimming pools, toilet seats — is explicitly ruled out by the textbook’s line that HIV “is not spread by mere touch or physical contact; it spreads only through body fluids.” Memorise the four and reject everything else.

Pathogenesis: from macrophage entry to TH collapse

Once HIV crosses a mucosal barrier or enters the bloodstream, the gp120 spike binds the CD4 receptor on a macrophage with the help of a chemokine co-receptor. Membrane fusion mediated by gp41 delivers the viral core into the cytoplasm. There the cargo of two RNA strands is set upon by reverse transcriptase, which writes a complementary DNA strand, degrades the RNA template and synthesises the second DNA strand to yield a double-stranded proviral DNA. Integrase then splices this proviral DNA into a host chromosome, where it sits as a latent template indistinguishable from cellular genes.

Host transcription machinery now produces fresh viral genomic RNA and the mRNAs for HIV proteins. Protease cleaves the precursor polyproteins into functional units, new virions assemble at the plasma membrane and bud out, each carrying a fresh envelope. The infected macrophage continues making virus for the life of the cell — NCERT calls it an “HIV factory.” The released progeny meet the body’s circulating helper T-lymphocytes, recognise CD4 there as well, and the cycle repeats inside the TH compartment. Each round burns out TH cells faster than they can be replaced, and over months to years the CD4 count crashes from the normal 800–1200 per microlitre to below 200 — the laboratory threshold for full-blown AIDS.

NEET 2023 directly probed this circuit by asking in which blood corpuscles does HIV replicate and produce progeny viruses — the answer the paper rewards is the helper T-lymphocyte (TH cell), as NCERT names that step explicitly. The macrophage is the earlier site, but the textbook reserves the phrase “produces progeny viruses” for TH cells, so when both appear as options pick TH.

The clinical course: time-lag, window period and AIDS

NCERT explicitly states that there is always a time-lag between HIV infection and the appearance of AIDS symptoms — usually 5–10 years, though it can range from a few months upwards. Inside that latent interval the person is infected, infectious, and often asymptomatic. Early in this phase comes the window period: the few weeks after exposure during which anti-HIV antibodies have not yet risen to ELISA-detectable levels, so a serological test reads negative even though the virus is replicating. Confirmation during the window period requires nucleic acid assays such as PCR that detect viral RNA directly.

As CD4 counts decline the patient begins to suffer recurrent fever, persistent diarrhoea and weight loss. With the helper T-lymphocyte arm of the immune system gutted, organisms the body once shrugged off establish themselves as opportunistic infections. NCERT names Mycobacterium (tuberculosis), various fungi, viruses and parasites such as Toxoplasma. It is these opportunistic infections, together with HIV-associated malignancies such as Kaposi’s sarcoma, that finally kill the patient — AIDS itself is the syndrome, the proximate causes of death lie one step downstream.

Diagnosis: ELISA and the antibody curve

The Enzyme Linked Immuno-Sorbent Assay is the textbook diagnostic for HIV. Patient serum is incubated in a well coated with HIV antigens; any anti-HIV antibodies present bind. A secondary enzyme-linked anti-human-Ig is added, then a chromogenic substrate; colour development indicates antibody presence and, by inference, infection. ELISA is sensitive, cheap and scalable, which is why national programmes use it for screening. Positive ELISA results are routinely confirmed by Western blot or a second ELISA on a different platform; PCR detects viral RNA directly and bypasses the window-period delay.

Treatment: antiretroviral therapy slows but does not cure

The standard pharmacological intervention is anti-retroviral therapy. The first drug in this class — and the one named most often in NCERT-aligned questions — is AZT, zidovudine, a nucleoside analogue that inhibits reverse transcriptase by mimicking thymidine and causing chain termination of nascent viral DNA. Modern regimens combine three or more drugs from at least two classes (reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors) to suppress viral replication below the limit of detection. This restores CD4 counts, dramatically reduces transmission and converts AIDS into a manageable chronic illness. NCERT, however, is uncompromising: anti-retroviral treatment “can only prolong the life of the patient but cannot prevent death, which is inevitable.” No combination therapy yet clears the integrated provirus from latent reservoirs, so cure is still beyond reach.

Prevention and the NACO–WHO axis

Because HIV spreads almost entirely through avoidable behavioural and procedural routes, prevention is treatable as an engineering problem with four levers. NCERT lists the levers in plain language and adds the slogan “don’t die of ignorance”. India’s National AIDS Control Organisation (NACO), coordinated with non-governmental organisations and the World Health Organisation, drives the national campaign. WHO sets global protocols and supplies surveillance.

Worked examples

Common confusion & NEET traps