Accumulation and breakdown of RNA-deficient intracellular virus particles in interferon-treated NIH 3T3 cells chronically producing Moloney murine leukemia virus

Abstract

Interferon treatment of NIH 3T3 cells chronically infected with Moloney murine leukemia virus inhibited about 95% of virus release. This inhibition was accompanied by a three- to twofold accumulation of intracellular virions. However, this accumulation could be demonstrated only be exogenous reverse transcriptase reaction assay or radioactive labeling of the assembled viral proteins. It could not be shown by the endogenous reverse transcriptase reaction assay, which depended on endogenous viral RNA, or by labeling the encapsidated viral RNA. It was therefore evident that most of the intracellular virions accumulated in interferon-treated cells were RNA deficient. Hybridization analysis revealed that these virions were deficient of genomic viral RNA, whereas size analysis by gel electrophoresis suggested that the deficiency of 4S RNA normally packaged in Moloney murine leukemia virus was even stronger. Our data also suggested that this RNA deficiency was not due to degradation of the encapsidated RNA, but more likely to a defect in virus assembly. RNA-lacking intracellular virions were unstable; they were found to collapse before being released.

Recombinant human interferon gamma suppresses HTLV‐III replication in vitro

“…Interferon has been reported to inhibit many animal retroviruses, including murine leukemia viruses, murine sarcoma virus and feline leukemia virus (Pitha et al, 1982; Aboud and Hassan, 1983;Sen et al, 1984). These effects are believed to be mediated in part by some critical alterations of viral transcription, translation, assembly and release in the host cells (Pitha el al., 1982; Aboud and Hassan, 1983). Gamma interferon is one of the antiviral/immunomodulatory agents which are capable of enhancing monocyte/macrophage Ia and FcR expression as well as monocyte-mediated cytotoxicity, release of interleukin-1, and priming for tumoricidal activity (Murray et al, 1984).…”

“…These compounds appeared to block viral infection at steps other than that of viral reverse transcriptase. Since interferon is known to suppress replication of many animal retroviruses either in vitro or in vivo (Pitha et al, 1982;Aboud and Hassan, 1983;Sen et al, 1984;Gresser et al, 1969), it might also inhibit HTLV-III/ LAV infections that are prevalent in AIDS patients. Indeed, Ho et al (1985) have reported that recombinant human interferon (rINF) alfa-A suppresses HTLV-carrying cell lines such as MT-4 were markedly permissive for HTLV-III/LAV infection and further showed a strong cytopathic effect (CPE) (Harada et al, 1985~).…”

Absence of xenotropic murine leukemia virus–related virus in blood donors in China

“…PCR products were separated on 1% agarose gel and stained with ethidium bromide. cDNA from NIH3T3 cells was used as positive control as described by Urisman and coworkers 1 because NIH3T3 cells contain Mus musculus endogenous proviruses that are highly homologous in sequence to XMRV 30,31 and can be amplified by the primers used for amplifying XMRV. Three negative controls (water without DNA template) were included in each experiment.…”

Immune Response to Mouse Mammary Tumor Virus in Mice Lacking the Alpha/Beta Interferon or the Gamma Interferon Receptor

“…In the murine AIDS (MAIDS) model, IFN-␥ contributes to the development of disease in MAIDSsusceptible mouse strains as shown through the use of neutralizing antibodies to IFN-␥ and of IFN-␥ 0/0 mice (16,57), while the ability to produce IFN-␣/␤ has been linked to a MAIDSresistant phenotype, although these data have not yet been corroborated by studies with IFN-␣/␤R 0/0 mice (22). Furthermore, the addition of exogenous IFN in cell culture had a variable effect on different retroviruses, with effects on early steps of the viral life cycle in some cases (5,15,51) and on late events in others (1,31,43,50).…”