Complement activation and immune complexes in early congenital HIV infection

Article Abstract:

It appears that the classical complement pathway is activated in babies infected with HIV and complement activation is not associated with the presence of immune complexes. Researchers tested blood samples from 14 HIV-infected babies and 33 HIV-exposed but uninfected babies for fragments produced during the activation of the classical and alternative complement pathways. Blood levels of the classical complement fragment C4d were greater in HIV-infected babies than in noninfected babies. Blood levels of the alternative complement fragment Bb were similar in both groups. An elevation in C4d levels occurred even in babies less than five months old, indicating that the process occurs very early. The only association between blood levels of immune complexes and complement activation occurred in babies older than 10 months.

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Diminished expression of cell-surface complement regulatory proteins in HIV-infected children and with HIV infection of peripheral blood mononuclear cells in vitro

Article Abstract:

The blood cells of HIV-infected children may be susceptible to destruction by HIV-induced activation of the blood's complement system, as is the case with adults. Researchers analyzed the sensitivity of two proteins that regulate the complement system, known as MCP and DAF, in 27 HIV-infected children and 12 HIV-uninfected children born to HIV-infected mothers. The expression of these proteins was decreased in HIV-infected children as measured by fluorescent intensity. The decreased expression of DAF was observed in children with advanced HIV disease. A reduction in complement-regulating proteins may prevent control of the complement system and lead to the destruction of infected cells. This could account for the drop in CD4 lymphocytes that occurs during HIV infection.

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Complement activation by HIV-1-infected cells: the role of transmembrane glycoprotein gp41

Article Abstract:

The gp41 transmembrane protein of HIV appears to activate some parts of the complement system. Researchers used a cell line that contained the glycoproteins present on the viral envelope. These cells activated the classical complement pathway by binding the C1q complement protein. The shedding of gp120 from the cells seemed to increase complement activation. This could explain why different viral isolates activate the complement system in different ways.

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