HIV co-infections (HBV, HCV, TB)

HIV-HBV Co-infection - Double Trouble Diagnosis

• Universal Screening: All HIV-positive individuals require HBV screening at initial diagnosis.
• Initial Serology Panel:
  • HBsAg (Hepatitis B surface antigen)
  • anti-HBs (Hepatitis B surface antibody)
  • anti-HBc (Total hepatitis B core antibody)
• Key Interpretations:
  • HBsAg (+): Active HBV infection.
  • anti-HBs (+) & anti-HBc (+/-): Immune (natural infection or vaccination).
  • Isolated anti-HBc (+): May indicate occult infection; check HBV DNA.

⭐ HIV infection significantly accelerates liver fibrosis progression in patients with chronic HBV, increasing the risk of cirrhosis and hepatocellular carcinoma by 3-6x.

HIV-HCV Co-infection - The Liver's Other Foe

• Epidemiology: Affects ~25% of HIV+ individuals, especially people who inject drugs (PWID). HIV co-infection increases the risk of chronic HCV to >80%.
• Pathophysiology: HIV accelerates HCV progression by impairing HCV-specific T-cell immunity.
  • This leads to faster liver fibrosis, earlier onset of cirrhosis, and a higher risk of hepatocellular carcinoma (HCC).
  • HCV itself does not accelerate HIV progression.
• Management:
  • Screen all HIV+ patients with an HCV antibody test; if positive, confirm with an HCV RNA viral load.
  • Initiate antiretroviral therapy (ART) for HIV first.
  • Once HIV is virologically suppressed, treat HCV with Direct-Acting Antivirals (DAAs), achieving >95% cure rates.
  • ⚠️ Monitor for drug-drug interactions between ART and DAAs.

⭐ In co-infected patients on effective ART, liver disease (cirrhosis, ESLD) surpasses AIDS-defining illnesses as a leading cause of mortality.

HIV-TB Co-infection - The Lethal Alliance

• HIV is the most potent risk factor for reactivating latent Mycobacterium tuberculosis (MTB), increasing annual risk from 5-10% (lifetime) to 5-10% (annually).
• Clinical presentation is stratified by CD4 count:
  • CD4 >200 cells/μL: Classic upper-lobe cavitary pulmonary TB.
  • CD4 <200 cells/μL: Atypical patterns; extrapulmonary disease (lymphadenitis, meningitis) and disseminated/miliary TB are common. Chest X-rays can be normal.

• Diagnosis: Tuberculin skin tests (TST) are unreliable due to anergy; Interferon-Gamma Release Assays (IGRAs) are preferred for latent TB. For active TB, nucleic acid amplification tests (NAAT) like Xpert MTB/RIF on sputum are crucial due to paucibacillary disease.

⭐ Paradoxical worsening of TB symptoms after starting antiretroviral therapy (ART) is the hallmark of TB-Immune Reconstitution Inflammatory Syndrome (TB-IRIS).

• Treatment Principles:

High‑Yield Points - ⚡ Biggest Takeaways

• HIV accelerates HBV and HCV progression to cirrhosis and liver cancer. Screen all new HIV patients for these co-infections.
• Tenofovir-based ART is dual-acting and preferred for HIV/HBV co-infection.
• Screen for latent TB in all HIV patients; a tuberculin skin test (TST) ≥5 mm is considered positive.
• Starting ART can trigger Immune Reconstitution Inflammatory Syndrome (IRIS), paradoxically worsening TB symptoms.
• Watch for drug-drug interactions between HCV direct-acting antivirals (DAAs) and antiretroviral therapy.