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Internal Medicine›Condition·Updated Apr 17, 2026·v1

HIV

HIV is a manageable chronic disease requiring lifelong antiretroviral therapy (ART). Management focuses on immediate treatment initiation, monitoring for immune recovery, and preventing opportunistic infections through CD4-stratified prophylaxis.

High Evidence170 references·5,941 words·24 min read·v1
HIVInfectious DiseaseARTAIDSInternal Medicine

Quick Reference

RxDrug of choiceDolutegravir (50 mg) + Tenofovir + Lamivudine (TLD)
AltAlternativesBictegravir-based regimens; Efavirenz (600 mg) if INSTIs are unavailable
⊘AvoidMonotherapy; delaying ART for baseline labs (except in CNS infections like Cryptococcus/TB)
DxTest of choice4th Generation HIV-1/2 Ag/Ab Immunoassay
ScKey scoreCD4+ T-cell count (Threshold <200 cells/µL for AIDS/Prophylaxis)
→When to referTreatment failure (VL >1000), suspected IRIS, pregnancy, or immunological non-response (CD4 <500 despite suppression)
Start ART on the day of diagnosis for all patients to achieve rapid viral suppression and prevent transmission (U=U).
Human Immunodeficiency Virus (HIV) is a chronic, progressive [[retrovirus]] infection that targets [[CD4+ T lymphocytes]], leading to profound immunosuppression and, if untreated, Acquired Immune Deficiency Syndrome (AIDS). The clinical landscape has shifted from managing a terminal illness to coordinating a chronic condition, where the primary goal is rapid and sustained viral suppression. Modern management centers on the "test and treat" strategy, emphasizing Same-Day Initiation (SDI) of [[antiretroviral therapy]] (ART) to improve long-term retention and prevent onward transmission. While life expectancy now approaches that of the general population for those with well-controlled disease, clinicians must remain vigilant for late presentations (CD4 <350 cells/µL), opportunistic infections, and the metabolic complications of long-term therapy. Success is defined by the "U=U" principle: Undetectable equals Untransmittable.

Overview and Recommendations

Background

  • •Recognize HIV as a zoonotic infection caused by two distinct types: HIV-1, the driver of the global pandemic, and HIV-2, which is less virulent and primarily restricted to West Africa. HIV-1 is further divided into groups, with Group M (Major) responsible for over 90% of global cases and subdivided into various clades like Subtype B (common in North America) and Subtype C (dominant in Southern Africa).
  • •Understand the primary mechanism of disease, which involves the depletion of through direct viral cytopathicity and chronic immune activation. This depletion leads to a predictable sequence of opportunistic infections and malignancies as the immune system fails to contain latent pathogens.
  • •Identify the three clinical phases of infection: the acute phase (initial 2–4 weeks with high viremia), the chronic phase (clinical latency lasting years), and AIDS (defined by a CD4 count <200 cells/µL or the presence of an AIDS-defining illness).
  • •Acknowledge the concept of the viral reservoir, which refers to anatomical compartments like the brain and lymphoid tissue where transcriptionally competent HIV genomes persist despite systemic viral suppression. This reservoir is the primary barrier to a functional cure.
  • •Note the changing epidemiology where HIV is increasingly concentrated in key populations, including men who have sex with men (MSM), people who inject drugs (PWID), and migrant populations, though heterosexual transmission remains the dominant route in many high-burden regions.

Evaluation

  • •Suspect (AHI) in patients presenting with a mononucleosis-like syndrome, including fever, lymphadenopathy, and a maculopapular rash, especially following high-risk exposure within the last 2–4 weeks. During this window, standard antibody tests may be negative, necessitating nucleic acid testing.
  • •Order a fourth-generation HIV-1/2 antigen/antibody immunoassay as the initial screening test. This assay detects both the p24 antigen (which appears early) and HIV antibodies, significantly shortening the diagnostic window compared to older tests.
  • •Confirm reactive screening results with an HIV-1/2 antibody differentiation immunoassay. If the differentiation assay is indeterminate or negative but the initial screen was positive, obtain an HIV-1 RNA nucleic acid test (NAT) to rule out acute infection.
  • •Obtain a baseline CD4+ T-lymphocyte count and plasma HIV RNA (viral load) immediately upon diagnosis. The CD4 count serves as the primary marker of immunological status, while the viral load provides a baseline for monitoring treatment efficacy.
  • •Perform genotypic resistance testing (GRT) before initiating ART to identify transmitted drug resistance. While ART should not be delayed for these results in a "test and treat" model, the regimen may need adjustment once results are available.
  • •Screen for co-infections that complicate management, including (HBV), (HCV), and syphilis. HIV co-infection increases the odds of HBV exposure by over six-fold and significantly accelerates the progression of liver fibrosis.
  • •Evaluate for latent or active (TB) using interferon-gamma release assays (IGRA) or tuberculin skin tests. In patients with advanced disease (CD4 <200 cells/µL), utilize urine TB-LAM antigen tests and Xpert Ultra to improve diagnostic yield.
  • •Assess for cryptococcal antigen (CrAg) in all patients with a CD4 count <200 cells/µL. Identifying asymptomatic cryptococcemia is vital, as these patients require pre-emptive antifungal therapy to prevent lethal meningitis.
  • •Calculate the nadir CD4 count, which is the lowest recorded count in the patient's history. A low nadir is a strong predictor of poor long-term immune recovery and a higher risk of non-AIDS-defining events.
  • •Screen for metabolic and organ dysfunction at baseline, including a lipid panel, hemoglobin A1c, and estimated glomerular filtration rate (eGFR). Certain ART components can exacerbate renal or cardiovascular risks.
  • •Identify "late presenters," defined as individuals diagnosed with a CD4 count <350 cells/µL or an AIDS-defining event. These patients require more intensive monitoring and immediate prophylaxis for opportunistic infections.
  • •Rule out pregnancy in all individuals of childbearing potential, as this influences the choice of the antiretroviral backbone and requires specific counseling regarding perinatal transmission prevention.

Management

  • •Implement Same-Day Initiation (SDI) of ART for all patients who are clinically stable and ready to start. Rapid initiation improves six-month retention and accelerates the time to viral suppression.
  • •Administer an Integrase Strand Transfer Inhibitor (INSTI)-based regimen as the preferred first-line therapy. The standard of care is Dolutegravir (DTG) 50 mg PO once daily combined with two Nucleoside Reverse Transcriptase Inhibitors (NRTIs), typically Tenofovir and Lamivudine.
  • •Utilize the fixed-dose combination of Dolutegravir 50 mg, Tenofovir Disoproxil Fumarate (TDF) 300 mg, and Lamivudine (3TC) 300 mg (TLD) as a highly effective, well-tolerated, once-daily single-tablet regimen.
  • •Consider dual therapy with Dolutegravir 50 mg and Lamivudine 300 mg for treatment-naïve patients without HBV co-infection and with a baseline viral load <500,000 copies/mL to reduce long-term drug exposure.
  • •Initiate primary prophylaxis for Pneumocystis jirovecii pneumonia (PCP) with Trimethoprim-sulfamethoxazole (TMP-SMX) 160/800 mg (one double-strength tablet) daily for all patients with a CD4 count <200 cells/µL.
  • •Manage asymptomatic cryptococcal antigenemia (CrAg+) with Fluconazole 800 mg daily for 2 weeks, followed by 400 mg daily for 8 weeks. In high-risk cases, a single high-dose of liposomal amphotericin B (10 mg/kg IV) may be added to improve survival.
  • •Monitor for (IRIS), a paradoxical worsening of infections after starting ART. In patients with TB, consider prophylactic Prednisone 40 mg/day for 2 weeks, then 20 mg/day for 2 weeks to reduce TB-IRIS incidence.
  • •Delay ART initiation for 2–4 weeks in patients with cryptococcal meningitis and 2–8 weeks in those with tuberculous meningitis to reduce the risk of life-threatening CNS-IRIS.
  • •Define viral suppression as a viral load <50 copies/mL. If the viral load remains ≥1000 copies/mL after 6 months of therapy, assess adherence and perform genotypic resistance testing to evaluate for treatment failure.
  • •Switch to a second-line regimen if resistance is confirmed, typically utilizing a Protease Inhibitor (PI) like Lopinavir/Ritonavir (LPV/r) 400/100 mg twice daily or a high-barrier INSTI.
  • •Transition stable, virologically suppressed patients to long-acting injectable Cabotegravir (600 mg) and Rilpivirine (900 mg) every 8 weeks if they prefer to avoid daily oral pills.
  • •Prescribe Pitavastatin 4 mg daily for primary cardiovascular prevention in patients aged 40–75, even with low traditional risk scores, as HIV-related inflammation significantly increases atherosclerotic risk.
  • •Avoid monotherapy or dual therapy (outside of specific approved combinations like DTG/3TC), as these strategies rapidly lead to the development of multi-drug resistance.
  • •Refer patients for specialized care if they are "immunological non-responders" (INR)—those who maintain viral suppression but fail to increase their CD4 count above 500 cells/µL after 2 years of ART.
  • •Monitor renal function and bone mineral density in patients on TDF-based regimens. If eGFR drops or bone loss is significant, consider switching to Tenofovir Alafenamide (TAF) or a tenofovir-sparing regimen.

Board Review — High Yield

  • •U=U — Undetectable equals Untransmittable; viral load <200 copies/mL prevents sexual transmission.
  • •4th Gen Assay — Detects p24 antigen and antibodies; reduces the window period to ~14-20 days.
  • •PCP Prophylaxis — Start TMP-SMX when CD4 <200 cells/µL; stop when CD4 >200 for >3 months on ART.
  • •IRIS — Paradoxical clinical worsening after ART initiation due to immune recovery; common with TB and Cryptococcus.
  • •Dolutegravir — Preferred INSTI due to high genetic barrier to resistance and once-daily dosing.
  • •START Trial — Proved that immediate ART initiation at any CD4 count reduces morbidity and mortality.
  • •Elite Controllers — Rare individuals who maintain undetectable viral loads without ART; still require monitoring.
  • •Mpox — Severity is CD4-dependent; patients with CD4 <200 are at high risk for necrotizing, fatal disease.

Deep Dive — Evidence Details

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