PubMed · 12632634
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J P Figueroa. 2002. Seeking a commitment for action: AIDS--2002.. https://pubmed.ncbi.nlm.nih.gov/12632634/
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Infection with HIV-1 is known to impair B cell function. To further elucidate the role of B cells during infection and tumorigenesis, we studied their numbers in cases of AIDS-related Kaposi's sarcoma (KS) during the HAART era. Patients with AIDS-related KS were identified from a database of 4,480 HIV-1 positive individuals and the incidence of KS and rate ratio was stratified according to nadir number of B cells, measured as the CD19 count. In an unadjusted model, we observed that lower B cell counts were associated with a statistically significant increased risk of KS development (p < 0.001). We also observed a trend toward increased counts during KS resolution. When adjusted for nadir CD4 count in a multi-variable model, higher B cell counts were protective against KS development (p = 0.015). These data highlight a potential role for B cells and therefore the humoral immune system in KS aetiopathogenesis.
We report on a patient affected by ICF syndrome (immunodeficiency, centromeric instability of chromosomes 1, 9 and 16 and facial dysmorphism), who presented with slowing in mentation, mild right hemiparesis and focal motor seizures. MRI study of the brain suggested a diagnosis of progressive multifocal leukoencephalopathy (PML), which was confirmed by JC virus DNA detection on CSF by polymerase chain reaction (PCR). This is a unique case of adult infective neurological complication described in ICF Syndrome.
The intimate relationship between the HIV-1 life-cycle and the activation state of cells supporting viral replication results in a dynamic interaction between coinfections and HIV-1 replication in dually infected people. The immunologic impact of recurrent coinfections has the potential to increase viral replication, viral genotypic heterogeneity and CD4 T lymphocyte loss, leading to accelerated decline in immune function, reduced survival and increased HIV-1 transmission risk. These effects may play a particularly significant role in the HIV-1 epidemic in sub-Saharan Africa. The mechanisms underlying these effects on virus-host dynamics are reviewed and data describing the impact of tuberculosis, malaria, schistosomiasis and genital ulceration on HIV-1 infection are presented.