Francesca Chiodi

TL;DR: According to their capacity to replicate in vitro, human immunodeficiency virus (HIV) isolates can be divided into two major groups, rapid/high and slow/low as mentioned in this paper.

TL;DR: It is concluded that reduction of memory B lymphocytes in HIV-1 infection correlates with defective humoral immunity and that hyperactivated naive B cells may represent the source of abnormal IgG production in HIV -1 infection.

TL;DR: It is suggested that HIV infection impairs maintenance of long-term serologic immunity to HIV-1-unrelated antigens and this defect is initiated early in infection, which may have important consequences for the response of HIV-infected patients to immunizations.

TL;DR: Examination of brains of asymptomatic HIV‐1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and felines infections suggest that, invasion of the CNS by HIV‐ 1 occurs at the time of primary infection and induces an immunological process in the central nervous system.

TL;DR: Ex vivo findings suggest that persistent T-cell activation may contribute to loss of memory B cells through upregulation of Fas/FasL on these cells and terminal differentiation into plasma cells.