[CD38 antigen as a marker for immunological follow-up in HIV-positive patients].

Background: HIV infection causes chronic activation of cytotoxic CD8+ T-lymphocytes, which is partly responsible for the hallmark of the disease--progressive loss of CD4+ T-lymphocytes. The aim of this study was to evaluate an influence of HIV infection and long-term antiretroviral therapy (HAART) on expression of the activation molecules CD38 on CD8+ T-lymphocytes.

Methods: A group of 16 HIV-positive patients treated with HAART was followed for 12 months.

Cd38 expression on Cd8+ T cells in Human immunodeficiency virus 1-positive adults treated with HAART.

The aim of this study was to assess whether the density of CD38 antigen expression on CD8+ T cells can be used as a marker of activation of the immune system in Human immunodeficiency virus 1 (HIV-1)-positive patients treated with highly active antiretroviral therapy (HAART). T cell subsets, expression of CD38 antigen on CD8+T cells, HIV-1 viral load and stage of the disease were analyzed at baseline and after 12 months of HAART in 24 HIV-1-infected patients. Our data showed that the use of HAART is effective in reducing plasma viral load and in achieving a stable CD4+ count and percentage of CD8+/CD38+ cells.

Daughter cell fusion and formation of polykaryons in a cold-resistant (CR) L cell variant.

A cold-resistant (cr) variant of mouse L fibroblasts called LC3, isolated by repeated cooling of the parent population for several weeks at 4 degrees C, differed from the wild-type cells in morphology and function. Microcinematographic records demonstrate that their motility is markedly reduced when compared with that of the L cells. They enter mitosis at 30 degrees C, at 37 degrees C and at 39 degrees C, but they finish cytodieresis only at 30 degrees C.