Decay‐accelerating factor (CD55) protects human immunodeficiency virus type 1 from inactivation by human complement

@article{Marschang1995DecayacceleratingF,
  title={Decay‐accelerating factor (CD55) protects human immunodeficiency virus type 1 from inactivation by human complement},
  author={Peter Marschang and Joseph G Sodroski and Reinhard W{\"u}rzner and Manfred Paul Dierich},
  journal={European Journal of Immunology},
  year={1995},
  volume={25}
}
HIV‐1 in contrast to animal retroviruses, is not lysed by human complement, but is readily inactivated by the sera from different animal species. To identify a possible species‐specific protection mechanism, HIV‐1 was expressed in cells of non‐human origin. Recombinant HIV‐1 virions that could encode the chloramphenicol acetyltransferase (CAT) protein were produced in African green monkey COS‐1 cells, mink cells and, as a control, in human HEp‐2 cells and were then used to infect CD4‐positive… Expand
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References

SHOWING 1-10 OF 58 REFERENCES
Host cell components affect the sensitivity of HIV type 1 to complement-mediated virolysis.
TLDR
The experiments show that the host cell type can substantially influence the susceptibility of HIV to complement-mediated virolysis and suggest that PI-linked complement control proteins play an important role in this resistance. Expand
The establishment of rodent cell lines persistently producing HIV-1.
TLDR
The transfection of murine and rat cells with an infectious clone of HIV-1 and a vector containing the chloramphenicol acetyl transferase gene demonstrated that some rodent cells have no inherent restriction to persistent and efficient production of infectious HIV- 1. Expand
Human T-cell leukaemia virus is not lysed by human serum
TLDR
It is reported here that, unlike other animal retroviruses, HTLV is not lysed by normal human serum—this might explain the infectivity and persistence of HTLV in humans. Expand
HIV and HIV-infected cells differentially activate the human complement system independent of antibody.
TLDR
It is shown that purified HIV as well as HIV-infected cells activate the complement system, and that C3 fragments deposited on the surface of HIV- infected cells are capable of mediating immune adherence to complement receptor-bearing cells, such as human erythrocytes and phagocytes. Expand
HIV‐I and HIV‐2 isolates differ in their ability to activate the complement system on the surface of infected cells
TLDR
Results suggest a role of gp41 for complement activation on HIV-infected cells as has been described previously for purified HIV. Expand
Neutralization of human immunodeficiency virus type 1 by complement occurs by viral lysis
TLDR
It is shown that complement can neutralize HIV via the classical complement pathway and that this neutralization occurs via C5b-9-mediated viral lysis and may play a major role in resistance to disease by lysing HIV and preventing infection of Fc- and complement receptor-positive cells, as well as CD4+ cells. Expand
HIV and complement: role of the complement system in HIV infection.
TLDR
Due to direct or indirect effects of HIV the complement system is in an activated state and the cellular expression of complement receptors as well as regulatory molecules is modified in the blood of HIV-infected patients. Expand
Inhibition of complement-mediated cytolysis by the terminal complement inhibitor of herpesvirus saimiri
TLDR
These data are the first to demonstrate a functional, virally encoded terminal complement inhibitor and suggest that HVSCD59 represents a humoral immune evasion mechanism supporting the lytic life cycle of HVS. Expand
Host cell modification of lymphocytic choriomeningitis virus and Newcastle disease virus altering viral inactivation by human complement.
  • R. Welsh
  • Biology, Medicine
  • Journal of immunology
  • 1977
TLDR
It is proposed that alterations in virulence dependent upon passage of the virus in cells or animals may be partially explained by changes in virus sensitivity to human serum inactivation. Expand
AIDS retrovirus (ARV-2) clone replicates in transfected human and animal fibroblasts.
TLDR
The results show that, whereas the primary block to ARV infection in certain cells may occur at the cell surface, intracellular mechanisms can also participate in controlling virus replication. Expand
...
1
2
3
4
5
...