“…Some of the earliest studies on HIV infection documented the ability of virus antigens to stimulate polyclonal activation of peripheral blood B cells (Schnittman et al, 1986). More recently, bystander killing of B cells in HIV-positive lymph nodes was reported to proceed by an apoptotic mechanism (Carbonari et al, 1997). Our studies of acute SHIV infection in macaques showed apoptotic death of B cells in parallel with CD4 + T cell depletion (M. Wallace & C. D. Pauza, unpublished).…”
Section: Implications For Viral Pathogenesis Mechanismmentioning
Clinical and laboratory markers of simian immunodeficiency virus (SIV) infection were studied during the first 3 months after intravenous inoculation of rhesus macaques. Virus-binding serum antibody titres were correlated strongly with disease progression (P 0n005) and were predictive of disease outcome by 7 weeks after inoculation. Low virusbinding serum antibody responses to SIV occurred
“…Some of the earliest studies on HIV infection documented the ability of virus antigens to stimulate polyclonal activation of peripheral blood B cells (Schnittman et al, 1986). More recently, bystander killing of B cells in HIV-positive lymph nodes was reported to proceed by an apoptotic mechanism (Carbonari et al, 1997). Our studies of acute SHIV infection in macaques showed apoptotic death of B cells in parallel with CD4 + T cell depletion (M. Wallace & C. D. Pauza, unpublished).…”
Section: Implications For Viral Pathogenesis Mechanismmentioning
Clinical and laboratory markers of simian immunodeficiency virus (SIV) infection were studied during the first 3 months after intravenous inoculation of rhesus macaques. Virus-binding serum antibody titres were correlated strongly with disease progression (P 0n005) and were predictive of disease outcome by 7 weeks after inoculation. Low virusbinding serum antibody responses to SIV occurred
“…In spleen white pulps HIV‐1‐specific T cells are highly compartmentalized [107]. In lymph nodes [108] and lungs [109] certain Vβ families were overrepresented in CD8+ T cells. T cells in labial salivary glands in patients with the sicca syndrome of HIV‐1 preferentially utilized Jβ1·2 [110].…”
“…One possible explanation for the slightly stronger correlation in HIV-1 infection is that the memory CD8 + T cell repertoire often tends to greater representation of certain Vβ families in both the Ki-67 + and Ki-67 -memory compartment, as has been seen in some (16,17) but not all studies (18).…”
Section: Il-15 Promotes Activation and Expansion Of Cd8 + T Cells In mentioning
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