Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1994 Dec;68(12):8001-7.
doi: 10.1128/JVI.68.12.8001-8007.1994.

Type C retrovirus inactivation by human complement is determined by both the viral genome and the producer cell

Affiliations
Comparative Study

Type C retrovirus inactivation by human complement is determined by both the viral genome and the producer cell

Y Takeuchi et al. J Virol. 1994 Dec.

Abstract

The inactivation of type C retroviruses by human serum may be a considerable impediment to the use of retroviral vectors in vivo for gene therapy. Here we show that virus inactivation is dependent both on the virus and on the cell line used to produce the virus. All viruses produced from murine NIH 3T3 or dog Cf2ThS+L- cells are sensitive to human serum. In contrast, those produced from mink Mv-1-Lu and human HOS or TE671 cells are at least partially resistant, with the exception of murine leukemia viruses. In particular, the feline endogenous virus RD114 is completely resistant to a panel of eight human sera when produced from Mv-1-Lu or HOS cells. This differential resistance is controlled by the viral envelope proteins. Virus inactivation can be correlated with the ability of the producer cells to be lysed by human serum. Inactivation of sensitive viruses requires the classical pathway of complement but does not require virion lysis.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Nature. 1975 Oct 16;257(5527):612-4 - PubMed
    1. J Virol. 1993 Nov;67(11):6737-41 - PubMed
    1. Virology. 1976 Oct 15;74(2):432-40 - PubMed
    1. J Immunol. 1977 Jan;118(1):348-54 - PubMed
    1. Nature. 1977 Mar 31;266(5601):458-9 - PubMed

Publication types

MeSH terms