CD4-Immunoglobulin G2 Protects Hu-PBL-SCID Mice against Challenge by Primary Human Immunodeficiency Virus Type 1 Isolates
AUTOR(ES)
Gauduin, Marie-Claire
FONTE
American Society for Microbiology
RESUMO
CD4-immunoglobulin G2 (IgG2) is a fusion protein comprising human IgG2 in which the Fv portions of both heavy and light chains have been replaced by the V1 and V2 domains of human CD4. Previous studies found that CD4-IgG2 potently neutralizes a broad range of primary human immunodeficiency virus type 1 (HIV-1) isolates in vitro and ex vivo. The current report demonstrates that CD4-IgG2 protects against infection by primary isolates of HIV-1 in vivo, using the hu-PBL-SCID mouse model. Passive administration of 10 mg of CD4-IgG2 per kg of body weight protected all animals against subsequent challenge with 10 mouse infectious doses of the laboratory-adapted T-cell-tropic isolate HIV-1LAI, while 50 mg of CD4-IgG2 per kg protected four of five mice against the primary isolates HIV-1JR-CSF and HIV-1AD6. In contrast, a polyclonal HIV-1 Ig fraction exhibited partial protection against HIV-1LAI at 150 mg/kg but no significant protection against the primary HIV-1 isolates. The results demonstrate that CD4-IgG2 effectively neutralizes primary HIV-1 isolates in vivo and can prevent the initiation of infection by these viruses.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=109861Documentos Relacionados
- Potent activity of 2'-beta-fluoro-2',3'-dideoxyadenosine against human immunodeficiency virus type 1 infection in hu-PBL-SCID mice.
- Role of interleukin-4 in human immunoglobulin E formation in hu-PBL-SCID mice.
- Transfer of Human CD4+ T Lymphocytes Producing Beta Interferon in Hu-PBL-SCID Mice Controls Human Immunodeficiency Virus Infection
- Selective Regulation of Human Immunodeficiency Virus-Infected CD4+ Lymphocytes by a Synthetic Immunomodulator Leads to Potent Virus Suppression In Vitro and in hu-PBL-SCID Mice
- Biochemical and functional characterization of xenoreactive natural antibodies in hu-PBL-SCID mice.