Mahadevan, A., Shankar, Susarla K., Satishchandra, Parthasarathy, Siddappa, N. B., Ranga, Udaykumar, Chickabasaviah, Yasha Thagadur, Santosh, Vani, Vasanthapuram, Ravi, and Nath, Avindra
Background: HIV-Clade C is the commonest subtype in Africa and Asia, but it remains unknown if this clade can invade the brain and cause neuronal damage. CNS opportunistic infections (OI) are common and frequently cause death. It remains unknown if OI can serve as a portal of HIV entry into the brain, putting patients at risk of developing HIV encephalitis and dementia. Methods: Formalin fixed tissues from 15 patients (toxoplasma encephalitis=5, tuberculous meningitis-5 and cryptococcal meningitis-5, head injury without OI-3) who came to autopsy at NIMHANS, Bangalore were immunostained for HIV-p24, CD68 and GFAP. All died within 6 months of onset of neurological symptoms and did not receive antiretroviral therapy. Results: Cerebral toxoplasmosis had the largest largest load of HIV infected cells around the foci of toxoplasma encephalitis. In tuberculosis, the HIV infected cells were prominent in the meningeal infiltrate with focal infiltration into the superficial cortex in few cases. Patients with cryptococcal meningitis had the least amount of inflammatory infiltrates restricted to meninges. HIV infected cells were occasionally present in the choroid plexus, suggesting that this could be a portal of entry for these cells into the sub-arachanoid space. Conclusions: The finding of large amounts of viral antigen within the brain in conjunction with various OI suggests that HIV dementia may supervene once the OI is successful treated. On the other hand, effective treatment of OI may inhibit OI induced pathology and help limit viral burden. This will have important public health implications in addressing the HIV epidemic in developing countries [ABSTRACT FROM AUTHOR]