HIV/AIDS: Diagnosis, Treatment & Prevention

HIV is a single-stranded RNA retrovirus (subtypes HIV-1 and HIV-2) that binds CD4 receptors on T-helper lymphocytes, monocytes, and dendritic cells via the CCR5 or CXCR4 co-receptor. Reverse transcriptase, integrase, and protease drive viral assembly, and integrated proviral DNA establishes a long-lived reservoir that current therapy can suppress but not eradicate. Untreated infection produces continuous CD4 depletion at roughly 50–100 cells/µL per year, leaving the host vulnerable to a defined set of opportunistic infections and malignancies once the count falls below the AIDS threshold.

AIDS (acquired immunodeficiency syndrome) is the late, immunocompromised stage—diagnosed by either CD4 below 200 cells/µL, a CD4 percentage below 14%, or an AIDS-defining illness regardless of count. With suppressive ART started early, most people never reach this stage; with delayed presentation, the same syndrome can present at first contact with the health service as Pneumocystis pneumonia, oesophageal candidiasis, or wasting. Treatment goals therefore split into immediate (durable virological suppression, immune recovery, prevent transmission) and longitudinal (cardiovascular, renal, bone, hepatic and oncology surveillance because the virus and the drugs both remodel risk).

Two staging frameworks dominate ward and clinic practice. The WHO clinical staging (1–4) is symptom-led and useful where CD4 is unavailable; the US CDC immunological staging uses CD4 cell count to drive prophylaxis and surveillance. Both should be documented at first encounter and revisited after any acute illness.

Children, pregnancy, and HIV-2 require modified thresholds (paediatric CD4 percentage in under-fives; HIV-2 has lower viral loads but slower CD4 decline)—follow local age-banded protocols rather than extrapolating adult cut-offs.

HIV is famously chameleonic. Most people pass through three overlapping clinical phases: acute (seroconversion) within weeks of infection, a chronic asymptomatic period that may run for years untreated, and finally symptomatic / AIDS illness driven by opportunistic infections and malignancies.

Early and atypical features

• Acute retroviral syndrome: fever, sore throat, lymphadenopathy, myalgia, oral ulcers, and a non-itchy maculopapular rash on the trunk—often dismissed as flu or glandular fever.
• Persistent generalised lymphadenopathy: rubbery, non-tender nodes >1 cm in two or more extra-inguinal sites for >3 months.
• Recurrent shingles (especially multidermatomal) or recurrent oral candidiasis in an otherwise healthy adult.
• Unexplained night sweats or thrombocytopenia at routine bloods.

Advanced disease

• Constitutional triad: unexplained weight loss, drenching sweats, and chronic fatigue.
• Respiratory: subacute dry cough, exertional dyspnoea, oxygen desaturation on exertion (PCP); cavitating upper-lobe infiltrate (TB).
• Neurological: cognitive slowing, seizures, focal deficit, or photophobia—think CNS opportunistic disease or HIV-associated neurocognitive disorder.
• GI: oesophageal odynophagia (candida or CMV), profuse non-bloody diarrhoea (Cryptosporidium, Microsporidium), painless perianal ulceration.
• Cutaneous: violaceous nodules of Kaposi sarcoma, multidermatomal zoster, recalcitrant seborrhoeic dermatitis on the central face.

HIV is transmitted through sexual fluids, blood, perinatal exposure, and breast milk. It is not transmitted through saliva, sweat, tears, casual contact, sharing crockery, mosquitoes, or toilet seats—an evidence point worth restating to anxious patients and ward staff alike. Transmission risk per exposure varies enormously: receptive anal intercourse without a condom is several orders of magnitude riskier than oral exposure; sharing injecting equipment carries roughly 1 in 150 per exposure; a needlestick from an HIV-positive source averages 0.3% but rises with hollow-bore, deep injury and high source viral load.

Coinfection profoundly modifies risk. Active gonorrhoea, genital herpes, and untreated pelvic inflammatory disease all raise transmission probability several-fold by inflaming mucosal barriers and recruiting CD4 cells to the site. Conversely, an undetectable viral load on suppressive ART removes sexual transmission risk entirely (U=U) and reduces vertical transmission to under 1% with appropriate intrapartum and infant care.

• Sexual: condomless receptive intercourse, multiple partners, transactional sex, partners of unknown status.
• Parenteral: shared syringes/needles, unsterile tattoo or body-piercing equipment, unscreened blood products (rare in countries with universal donor screening).
• Vertical: in utero, intrapartum, or via breast milk—virtually eliminated when maternal viral load is undetectable.
• Occupational: percutaneous sharps injury or mucosal splash with infected blood—prevention via safer engineering and PEP after exposure.

Modern HIV diagnosis follows a tiered algorithm: a fourth-generation Ag/Ab combination assay (detects p24 antigen plus IgG/IgM antibodies) shortens the window period to ~14–21 days; reactive samples reflex to an HIV-1/HIV-2 differentiation assay, and any discordant or early result is confirmed with a quantitative HIV-1 RNA. Point-of-care tests are useful for outreach but should be confirmed by a laboratory algorithm before disclosure or treatment.

Once infection is confirmed, the baseline panel anchors care:

• HIV serology (confirmatory differentiation) plus quantitative HIV-1 RNA and CD4 count/percentage.
• Genotypic resistance test before first-line therapy where local prevalence of transmitted resistance justifies it.
• HLA-B*5701 if abacavir is being considered (hypersensitivity screen).
• Coinfection screen: HBsAg/anti-HBc/anti-HBs, HCV antibody (with reflex RNA), syphilis serology, gonorrhoea/chlamydia NAAT at relevant sites.
• Latent TB screen (interferon-gamma release assay or tuberculin skin test) plus a baseline chest X-ray when TB risk is non-trivial.
• Baseline CBC, metabolic panel, liver function tests, eGFR, urine ACR, fasting lipids, and pregnancy test where applicable.
• Cervical screening with cytology; consider anal cytology in MSM with low CD4 nadir.

Sample handling matters: prevent contamination by following hand hygiene before and after venepuncture, label tubes at the bedside, and align specimen collection with laboratory cut-off windows—plasma HIV-1 RNA tubes have a finite stability and a delayed centrifugation can spuriously lower the result.

1. Detect — Offer testing on universal opt-out basis in any setting where local prevalence supports it; reflex any reactive Ag/Ab result through the lab algorithm before disclosure.
2. Stratify — Confirm CD4 count, HIV-1 RNA, coinfection screen, pregnancy, and mental-health/social context that may affect adherence.
3. Treat — Start ART rapidly (same day where possible); pick a regimen aware of HBV status, pregnancy, renal/hepatic function, and HLA-B*5701; defer briefly only for cryptococcal or TB meningitis.
4. Prophylax — Add co-trimoxazole if CD4 <200; add MAC prophylaxis if CD4 <50 and not yet on suppressive ART; add isoniazid preventive therapy after active TB excluded.
5. Surveil — HIV-1 RNA at 4–8 weeks then 3–6 monthly; CD4 every 3–6 months until stable then yearly; renal, lipid, bone, and cervical screening per local cadence; reconcile medications at every visit because antiretrovirals interact with statins, anticonvulsants, hormonal contraception and many over-the-counter products.
6. Escalate — Any new neurology, hypoxia, sepsis physiology, IRIS, or pregnancy with detectable viral load near term—activate the appropriate pathway; blood cultures precede antibiotics in the febrile patient.

The diagnosis is usually serological once asked, but the presenting syndrome can mimic many things. Hold the alternatives in mind so HIV is not over- or under-called.

• Mononucleosis (EBV/CMV)—shares fever, pharyngitis, lymphadenopathy and rash, but heterophile antibodies and viral PCR distinguish.
• Secondary syphilis—palmoplantar rash, snail-track ulcers, generalised lymphadenopathy; co-test always (syphilis-HIV co-infection is common).
• Disseminated tuberculosis—chronic fevers, weight loss, sweats; consider in any low-CD4 host. Coexists with HIV; treat both, sequence carefully.
• Lymphoma (Hodgkin or non-Hodgkin)—B-symptoms with lymphadenopathy; biopsy is decisive. HIV both raises lymphoma risk and shares the symptom set.
• Drug reactions and serum sickness—fever and rash on a new medication; full medication history helps.
• Acute viral hepatitis—prodromal fever and malaise; LFTs, viral serology, and ultrasound separate from HIV; HCV coinfection is frequent in people who inject drugs.
• Idiopathic CD4 lymphocytopenia—rare, repeated low CD4 in serologically negative people; HIV-1/2 RNA confirms exclusion.

Combination antiretroviral therapy (ART)

First-line therapy in most adult guidelines is an integrase strand transfer inhibitor (INSTI) backbone—commonly bictegravir or dolutegravir—paired with two nucleoside reverse-transcriptase inhibitors (tenofovir alafenamide or disoproxil with emtricitabine or lamivudine). Single-tablet regimens improve adherence; two-drug regimens (e.g. dolutegravir/lamivudine) are option for selected, hepatitis-B-negative, suppressed patients. Long-acting injectable cabotegravir/rilpivirine every 1–2 months is licensed for virologically suppressed adults who prefer injections to daily pills.

Choose the backbone with hepatitis-B status, pregnancy plans, renal function and bone risk in mind. Tenofovir disoproxil is potent and HBV-active but penalises bone and proximal tubules; tenofovir alafenamide is gentler renally but raises lipids; abacavir needs HLA-B*5701 negative and is best avoided in high cardiovascular risk; efavirenz is increasingly displaced by integrase inhibitors but remains a workhorse where INSTIs are unavailable. Counsel on weight gain (notable with INSTI + tenofovir alafenamide), neuropsychiatric effects (efavirenz), and integrase-related insomnia.

Opportunistic infections — recognise and treat

Special populations

• Pregnancy: continue or start ART throughout; aim for undetectable viral load by 34–36 weeks; some integrase inhibitors are now preferred but periconception data continue to evolve—use the local antenatal HIV protocol.
• Renal disease: avoid tenofovir disoproxil if eGFR <60 mL/min/1.73 m²; consider tenofovir alafenamide or non-tenofovir backbones in advanced chronic kidney disease.
• Hepatitis-B coinfection: include two HBV-active drugs (tenofovir + emtricitabine or lamivudine); never stop them abruptly—flares are dangerous.
• Older adults / polypharmacy: integrase inhibitors interact with calcium, magnesium and antacids (chelation); statins, anticonvulsants and hormonal contraception need explicit review.
• Children and adolescents: weight-band dosing, fixed-dose combinations where licensed, transition planning to adult services; addresses psychosocial barriers as actively as the regimen.

• Confidentiality: HIV status is sensitive information—document on the medical record per local data-protection law, never on a whiteboard or shared kardex; partner notification is the prescriber/health-protection role, not bedside conversation.
• Adherence support: ask about adherence in normalising terms (“how many doses have you missed in the last week?”), use pillboxes, dose-time alarms, and pharmacy-led medicines optimisation; one missed integrase-inhibitor dose is rarely catastrophic, but repeated lapses select resistance.
• Drug interactions: integrase inhibitors and protease inhibitors interact widely—check the Liverpool HIV interactions database (or the equivalent local resource) before adding antacids, anticonvulsants, statins, methadone, or hormonal contraception.
• Vaccination: inactivated influenza, pneumococcal (PCV20 or PCV15+PPSV23), COVID-19, hepatitis A and B, HPV up to age 26 (or 45 with risk), MenACWY/Men B for those at risk; live vaccines need CD4 review.
• Stigma awareness: language matters—“person living with HIV”, not “HIV patient”; “undetectable”, not “low viral load”; avoid the word “clean” for HIV-negative status.
• Universal precautions every time: HIV does not change wound dressing, suctioning or IV care—the same standard precautions apply to every patient regardless of diagnosis. Disclose only on a need-to-know clinical basis.

Bedside monitoring checklist

• NEWS2 or local early-warning score every shift; escalate any rise of ≥2 with the HIV team.
• Daily neurological observations (GCS, pupils, focal exam) when CNS opportunistic disease is on the differential.
• Strict input/output and weight if diarrhoea, fever, or amphotericin/aminoglycoside therapy.
• Tongue and mouth check daily for new candida; skin survey for new rash, zoster or Kaposi lesions.
• Blood-glucose and ketone monitoring if on integrase-inhibitor + tenofovir alafenamide and weight is climbing.
• Capture vital signs after every dose of IV pentamidine, amphotericin or first-dose ART—especially blood pressure and oxygen saturation.

• Opportunistic infections—as above; recurrence indicates failed adherence or resistance.
• HIV-associated malignancies—Kaposi sarcoma, primary CNS or systemic non-Hodgkin lymphoma, cervical and anal cancer, and (with HBV/HCV coinfection) hepatocellular carcinoma.
• Cardiometabolic—accelerated atherosclerosis, weight gain on integrase + tenofovir alafenamide, dyslipidaemia, insulin resistance, hypertension.
• Renal—tenofovir-related tubular dysfunction, HIV-associated nephropathy, cirrhosis-related hepatorenal physiology when HCV/HBV coinfected.
• Bone—reduced BMD, fragility fracture risk; review tenofovir disoproxil exposure.
• Neurocognitive—HIV-associated neurocognitive disorder (HAND) ranges from asymptomatic impairment to dementia; distal symmetrical peripheral neuropathy is common, especially historically with stavudine/didanosine but still seen with high disease burden.
• Mental health—depression, anxiety, substance use disorders are 2–4× more prevalent and worsen adherence.
• IRIS—paradoxical worsening of an existing OI within weeks of effective ART, especially TB and cryptococcosis; treat the OI, support the patient, rarely stop ART.

Prevention sits on three pillars: treatment-as-prevention (U=U), pre-exposure prophylaxis (PrEP) for HIV-negative people at substantial ongoing risk, and post-exposure prophylaxis (PEP) after an isolated high-risk event. Behavioural prevention (condoms, sterile injecting equipment, harm-reduction services) and structural interventions (opioid agonist therapy, needle-and-syringe programmes) sit alongside.

PrEP — pre-exposure prophylaxis

• Oral daily tenofovir disoproxil/emtricitabine (or tenofovir alafenamide/emtricitabine) for adults at risk; on-demand “2-1-1” dosing is an option for cisgender men who have sex with men in selected guidelines.
• Long-acting injectable cabotegravir every 8 weeks (after lead-in) is licensed for adults and adolescents weighing ≥35 kg.
• Confirm HIV-negative status before each dispense, recheck every 3 months on oral PrEP and per protocol on injectable; screen renal function, hepatitis B, and STIs.
• Counsel on side-effect profile, need for adherence, and the difference between PrEP and ART (do not start PrEP if HIV is undetected but present—risk of resistance).

PEP — post-exposure prophylaxis

• Eligible: condomless receptive intercourse with a partner of unknown HIV status, sharing of injecting equipment, percutaneous or mucosal exposure to HIV-positive blood.
• Three-drug regimen (commonly tenofovir/emtricitabine + dolutegravir or raltegravir) for 28 days; start within hours, no later than 72 hours from exposure.
• Baseline HIV test, hepatitis B/C, syphilis, pregnancy test; repeat HIV at 4–6 weeks and (per local protocol) 12 weeks after PEP completion.
• Document every timestamp—exposure, first dose, follow-up appointments—occupational health and infection-control implications follow.

Other prevention work that is often nurse-led

• Universal infant hepatitis B vaccination; HPV vaccination per local schedule; meningococcal vaccination in MSM clusters.
• STI partner notification, contact tracing, and routine screening on a 3- to 12-month cadence depending on risk.
• Vertical-transmission prevention: antenatal HIV testing for every pregnancy, ART throughout, infant prophylaxis, and a feeding plan that fits the local context.
• Engineering and behaviour at the bedside: safety-engineered sharps, double-gloving for high-risk procedures, and disciplined isolation precautions for transmissible co-infections (e.g. pulmonary TB or measles), not for HIV per se.

People diagnosed early and started on suppressive ART approach the life expectancy of their HIV-negative peers, modulated by the coexisting cardiovascular, renal, hepatic and oncology profile. Late presentation (CD4 below 200 or AIDS-defining illness at first contact) carries a several-fold higher one-year mortality, almost entirely driven by opportunistic infections in the first months. The trajectory therefore depends as much on engagement with care, adherence support and prevention of comorbid disease as on the antiretrovirals themselves.

Realistic counselling avoids two opposite errors. Telling a newly diagnosed person that HIV is “just a chronic disease” minimises the work of adherence, stigma, and surveillance; telling them that “AIDS” still implies imminent death misrepresents modern outcomes. The accurate message is that durable virological suppression is the lever, U=U is the practical promise, and lifelong follow-up is the price.

Spotting subtle deterioration in someone with HIV often begins at handover. New breathlessness in a patient who walked in last week, a fall in oxygen saturation on exertion, or a “mild headache” that the patient now wants to lie down with—these are the cues that prompt early imaging, lumbar puncture, or a senior review rather than a paracetamol and a reassurance. Routine pain assessment may unmask oesophageal candidiasis (odynophagia), CMV colitis (cramping diarrhoea), or zoster prodrome before the rash appears.

Communication challenges are common. People living with HIV may have learned to under-report symptoms to gatekeep stigma; a non-HIV-trained ward nurse may inadvertently broadcast diagnosis through medication trolleys or bedside conversation. Use the patient’s preferred language, ask before discussing diagnosis with relatives, and capture the conversation in handover in clinically necessary terms only.

Whilst awaiting senior review: secure IV access, send paired lactate and blood cultures, treat hypoglycaemia, give controlled oxygen to maintain target SpO₂, and prepare the team for early imaging. In a patient with profound CD4 depletion, presume the most dangerous diagnosis until evidence excludes it.

These NCLEX-style clinical judgment practice items focus on the nursing priorities for this condition — recognise cues, escalate red flags, take safe action and evaluate outcomes (NCSBN Clinical Judgment Measurement Model) — through Priority FIRST, SATA, deterioration trends, multi-patient triage, ordered response, matrix matching and a compact cloze on the topic of HIV/AIDS recognition (acute retroviral syndrome, AIDS-defining illnesses), structured rapid-ART start, opportunistic-infection prophylaxis, PrEP/PEP timing and the IRIS / PCP / cryptococcal-meningitis red flags.