Apoptosis e infección por el virus de la inmunodeficiencia humana (HIV). / [Apoptosis and human immunodeficiency virus infection (HIV]

Generalized activation of the immune system after HIV infection leads to an exacerbation of all apoptotic mechanisms. CD4+, CD8+ T lymphocytes and B lymphocytes are sensitized to apoptotic stimuli. Macrophages are important in the removal of apoptotic cells, they prevent apoptotic cell accumulation during in vitro culture and they may lead to enhanced CD4+ T lymphocyte cell death through indirect mechanisms. A simple procedure for prolonged culture of peripheral blood mononuclear cells from HIV+ patients is discussed, in relation to its convenience to evaluate apoptosis, cell to cell interaction and HIV replication in the absence of exogenously added stimuli or co-culture of allogeneic cells. In this system, HIV replication takes place primarily in cells of macrophage lineage that may be activated into differentiation through removal of apoptotic debris during the culture.

Macrófagos infectados por HIV aislados de pacientes HIV+ con carga viral indetectable luego del tratamiento antirretroviral combinado. / [HIV infected macrophages isolated from HIV+ patients with undetectable viral load undergoing combined antiretroviral treatment]

A new method of culture of peripheral blood leukocytes (PBMC) from HIV+ patients, in the absence of exogenous stimuli (allogeneic cells or cytokines) (PBMC w/s) was used for the detection of persistent viral infection in HIV patients who had undergone successful highly active antiretroviral therapy (HAART) lowering their viral burden to undetectable levels (< 50 RNA copies/ml). Infected cells were always of the monocyte/macrophage lineage (M). No infection could be detected in these patients using the classical system (co-culture with HIV-CMP activated with PHA and IL-2). Differences in the class of target cells (higher proportion of proliferating M and CCR5 expressing cells in the PBMC w/s system than in PBMC-PHA cultures) may determine the relative sensitivity of each technique to achieve successful isolation of HIV from different patients.

Apoptosis e infección por el virus de la inmunodeficiencia humana (HIV) / [Apoptosis and human immunodeficiency virus infection (HIV]

Generalized activation of the immune system after HIV infection leads to an exacerbation of all apoptotic mechanisms. CD4+, CD8+ T lymphocytes and B lymphocytes are sensitized to apoptotic stimuli. Macrophages are important in the removal of apoptotic cells, they prevent apoptotic cell accumulation during in vitro culture and they may lead to enhanced CD4+ T lymphocyte cell death through indirect mechanisms. A simple procedure for prolonged culture of peripheral blood mononuclear cells from HIV+ patients is discussed, in relation to its convenience to evaluate apoptosis, cell to cell interaction and HIV replication in the absence of exogenously added stimuli or co-culture of allogeneic cells. In this system, HIV replication takes place primarily in cells of macrophage lineage that may be activated into differentiation through removal of apoptotic debris during the culture.

Carga viral en líquido cefalorraquídeo de pacientes hemofilicos HIV-1 positivos bajo tratamiento con HAART. / [Cerebrospinal fluid viral load in HIV-1 positive hemophilic patients treated with HAART]

As HIV seropositive patients with undetectable CSF viral load have a lower likelihood of developing neurologic disease, the determination of CSF viral load levels may be useful to evaluate the efficacy of HAART. We compared plasma viral load levels with HIV-1 RNA CSF levels in 18 hemophilic patients without neurocognitive involvement under HAART. We detected a significant correlation between plasma viral load levels and CSF viral load levels. Fourteen patients with undetectable plasma viral load had undetectable RNA HIV-1 CSF levels as well. Four patients with detectable plasma viral load had detectable HIV-RNA in CSF, but the latter were significantly lower. Viral load is usually lower in non-blood fluids and HAART decreases the viral load in CSF as well as in blood.