scholarly journals Vitamin D Inhibits Human Immunodeficiency Virus Type 1 and Mycobacterium tuberculosis Infection in Macrophages through the Induction of Autophagy

2012 ◽  
Vol 8 (5) ◽  
pp. e1002689 ◽  
Author(s):  
Grant R. Campbell ◽  
Stephen A. Spector
Keyword(s):  
Vitamin D ◽  
Human Immunodeficiency Virus ◽  
Mycobacterium Tuberculosis ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Tuberculosis Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Immunodeficiency Virus

scholarly journals Human Immunodeficiency Virus Type 1 (HIV-1)Quasispecies at the Sites of Mycobacterium tuberculosis InfectionContribute to Systemic HIV-1 Heterogeneity

2002 ◽  
Vol 76 (4) ◽  
pp. 1697-1706 ◽  
Author(s):  
Kalonji R. Collins ◽  
Miguel E. Quiñones-Mateu ◽  
Mianda Wu ◽  
Henry Luzze ◽  
John L. Johnson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mycobacterium Tuberculosis ◽  
Pleural Fluid ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Mononuclear Cells ◽  
Pleural Space ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT We have recently reported an increased heterogeneity in the human immunodeficiency virus type 1 (HIV-1) envelope gene (env) in HIV-1-infected patients with pulmonary tuberculosis (TB) compared to patients with HIV-1 alone. This increase may be a result of dissemination of lung-derived HIV-1 isolates from sites of Mycobacterium tuberculosis infection and/or the systemic activation of the immune system in response to TB. To distinguish between these two mechanisms, blood and pleural fluid samples were obtained from HIV-1-infected patients with active pleural TB in Kampala, Uganda (CD4 cell counts of 34 to 705 cells/μl, HIV-1 plasma loads of 2,400 to 280,000 RNA copies/ml, and HIV-1 pleural loads of 7,600 to 4,500,000 RNA copies/ml). The C2-C3 coding region of HIV-1 env was PCR amplified from lysed peripheral blood mononuclear cells and pleural fluid mononuclear cells and reverse transcriptase-PCR amplified from plasma and pleural fluid HIV-1 virions of eight HIV-1 patients with pleural TB. Phylogenetic and phenetic analyses revealed a compartmentalization of HIV-1 quasispecies between blood and pleural space in four of eight patients, with migration events between the compartments. There was a trend for a greater genetic heterogeneity in the pleural space, which may be the result of an M. tuberculosis-mediated increase in HIV-1 replication and/or selection pressure at the site of infection. Collectively, these findings suggest that HIV-1 quasispecies in the M. tuberculosis-infected pleural space may leak into the systemic circulation and lead to increased systemic HIV-1 heterogeneity during TB.

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