PubMed · 12289864
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1995-06-12. United Nations forms program to combat AIDS.. https://pubmed.ncbi.nlm.nih.gov/12289864/
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Unilateral retrobulbar optic neuritis developed in a 43-year-old man with acquired immune deficiency syndrome (AIDS). This was secondary to varicella zoster virus (VZV) as confirmed by cerebrospinal fluid (CSF) polymerase chain reaction (PCR) detection of VZV in the cerebrospinal fluid. There was no typical cutaneous infection and no evidence of retinitis. The onset of unexplained visual loss due to optic neuritis in HIV positive individuals may be due to VZV infection. Prompt recognition, and early intervention with antiVZV therapy may preserve vision. Retrobulbar optic neuritis secondary to VZV infection should be considered in immunocompromised patients even in the absence of cutaneous or retinal lesions. Previous cases are reviewed and the varied nature of viral transport in the nervous system is noted.
A prior diagnosis of HIV increases the risk of lymphoma between 150 to 250- fold, depending on the subtype, as compared with the risk observed in the general population. The advent of highly active anti-retroviral therapy (HAART) has seen a dramatic reduction in AIDS morbidity and a modest reduction in the incidence of opportunistic infections along with a corresponding reduction in Kaposi's sarcoma. There has not, however, been a clear reduction in the incidence of lymphoma. As HAART therapy continues to improve in the Western world, the morbidity of HIV infection is beginning to shift from AIDS to other associated illness such as lymphoma. The treatment and etiology of lymphoma is a burgeoning issue in the care of HIV positive populations. This review will provide a basic overview of the association between HIV and lymphoma.
Previous studies have shown that the transmembrane (TM) domain of the subtype B Vpu enhances virion release from cells and some studies have shown that this domain may form an oligomeric structure with properties of an ion channel. To date, no studies have been performed to assess the role of this domain in virus pathogenesis in a macaque model of disease. Using a pathogenic molecular clone of simian human immunodeficiency virus (SHIVKU-1bMC33), we have generated a novel virus in which the transmembrane domain of the Vpu protein was scrambled but maintained hydrophobic in nature (SHIVTM), which presumably would disrupt any ion channel TM properties of this protein. Vectors expressing the Vpu as a fusion protein with the enhanced green fluorescent protein (VpuTMEGFP) indicate that it was transported to the same intracellular compartment as the unmodified Vpu protein but did not down-regulate cell surface expression of CD4. To assess the pathogenicity of SHIVTM, three pig-tailed macaques were inoculated with the SHIVTM and monitored for 6-8 months for CD4+ T cell levels, viral loads and the stability of the sequence of the vpu gene. Our results indicated that unlike the parental SHIVKU-1bMC33, inoculation of macaques with SHIVTM did not cause a severe CD4+ T cell loss over the course of their infections. Sequence analysis of the vpu gene analyzed from sequential PBMC samples derived from macaques revealed that the scrambled TM was stable during the course of infection. At necropsy, examination of tissues revealed low viral loads and none of the pathology commonly observed in lymphoid and non-lymphoid tissues following inoculation with the pathogenic parental SHIVKU-1bMC33 virus. Thus, these results show for the first time that the TM domain of Vpu contributes to the pathogenicity of SHIVKU-1bMC33 in pig-tailed macaques.