TAT and Opportunistic infection: Histopathological studies have demonstrated cerebellar white matter and cortical degeneration in the absence of opportunistic infections, pointing toward a direct neurotoxic effect of the virus.[22] Notably, several HIV envelope proteins—such as gp120, gp41, and Tat—have been implicated in neuronal damage, particularly within the cerebellar dentate and inferior olivary nuclei.[23] In addition, the viral accessory protein Vpr has been shown to induce apoptosis in cerebellar neurons, further supporting a pathogenic role for direct viral toxicity.[24].