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Query: UNIPROT:Q17RS7 (Gen)
 130,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Induction of the major stress response in chick embryo fibroblasts, which follows infection at 38.5 degrees C with the herpes simplex virus mutant tsK, was investigated. Synthesis of cellular stress proteins occurred only when the mutant form of an immediate early polypeptide, Vmw175, was overproduced. Infection with mutant in 1411, which has an amber (TAG) termination signal inserted between codons 83 and 84 of the gene encoding Vmw175 and therefore specifies a truncated portion of the polypeptide, failed to stimulate stress protein synthesis. The results suggested that the presence of abnormal forms of Vmw175 at high concentrations was the signal for induction of the stress response in tsK-infected cells.
J Gen Virol 1987 Sep
PMID:Abnormal forms of the herpes simplex virus immediate early polypeptide Vmw175 induce the cellular stress response. 282 Nov 79

Organ explants of porcine ileum were cultured in different media for up to 48 h. Tissue preservation was evaluated by light microscopy and by transmission and scanning electron microscopy. Cellular structure was well maintained after incubation for 48 h in CMRL-1066 supplemented with insulin and cortisone. Explants of absorptive or lymphoid tissue from young or adult pigs were incubated with either coxsackievirus B5 (which is infectious for swine) or human poliovirus type 1 (which served as a control) for 24 h at 37 degrees C. Progeny virus was detected by plaque assay. Replication was most evident in the absorptive tissue explants from young pigs. In tissues from adults, replication occurred equally well in absorptive and lymphoid tissues. Infection in explants was inefficient, and the yield of progeny virus was low.
J Gen Virol 1987 Sep
PMID:Enterovirus replication in porcine ileal explants. 282 Nov 87

Juvenile rhesus macaques 6 to 18 months of age were experimentally infected by intravenous inoculation with the simian immunodeficiency virus (SIV), the T cell-tropic retrovirus of monkeys related to the human acquired immunodeficiency syndrome (AIDS) virus HIV. The SIV used for inoculation was grown either in normal human peripheral blood lymphocytes in the presence of interleukin 2 or in the human tumour cell line HUT-78. Eight of the macaques died 129 to 352 days post-inoculation with a variety of clinical and pathological findings paralleling those of AIDS in humans. However eight other animals became persistently infected for prolonged periods; these eight macaques remained alive at 537 and 820 days post-inoculation despite persistent lymphadenopathy and our continued ability to isolate SIV. The ability of these monkeys to survive infection correlated directly with the strength of their antibody response to SIV. Infection was also established in macaques using approximately 100 tissue culture infectious doses of HUT-78-grown SIV. There was no correlation between the dose of virus inoculum and either the strength of the antibody response or clinical outcome. These results demonstrate that SIV infection of macaques can be used not only to study acute AIDS but also to mimic the long-term persistent infection seen in carriers of HIV.
J Gen Virol 1987 Dec
PMID:Long-term persistent infection of macaque monkeys with the simian immunodeficiency virus. 282 56

Infection of Vero cells with Tacaribe virus stocks containing a high ratio of standard (plaque-forming) viruses to defective interfering particles (DIP) induced inhibition of the host cell Ca2+ ATPase (Ca2+ pump) and the ouabain-sensitive Na+/K+ ATPase (Na+/K+ pump). The Mg2+ ATPase which is not involved in cation transport was not affected. The presence of DIP in the inocula protected the cells from alteration of the transport-associated ATPases induced by standard viruses.
J Gen Virol 1988 Apr
PMID:Tacaribe virus infection may induce inhibition of the activity of the host cell Ca2+ and Na+/K+ pumps. 283 72

Infection of tertiary-passaged mouse embryo fibroblasts by four flaviviruses, West Nile (WNV), Kunjin, Murray Valley encephalitis and Japanese B encephalitis, resulted in a six- to 10-fold increase in the expression of individual H-2K and H-2D class I major histocompatibility complex (MHC) antigens 16 to 48 h after infection. The mechanism(s) by which flaviviruses increased antigen expression has not been fully elucidated, but appears to be mediated partly independently of interferon-beta (IFN-beta) secretion, as anti-IFN-alpha beta antibodies partially inhibited the WNV-induced increase but totally prevented increases caused by the addition of (i) pure IFN-beta, (ii) IFN-beta-containing supernatants from WNV-infected mouse embryo fibroblasts (MEF), or (iii) polyinosinic-polycytidylic acid. Actinomycin D treatment of MEF, which inhibited mRNA synthesis by greater than 90% as determined by [3H]uridine uptake, totally inhibited the increased MHC expression caused by WNV infection. Thus, the increase in class I MHC antigen expression following infection is dependent upon cellular RNA synthesis.
J Gen Virol 1988 Oct
PMID:Interferon-independent increases in class I major histocompatibility complex antigen expression follow flavivirus infection. 284 65

The role of gangliosides in rabies virus infection of chick embryo-related (CER) cells was investigated. Cultured cells were pretreated with neuraminidase to render the cells transiently non-susceptible to viral infection. Incubation of these desialylated cells with gangliosides allowed them to incorporate exogenous gangliosides and they recovered their susceptibility to rabies virus infection. Infection of CER cells was monitored by specific fluorescence 24 h after virus inoculation. The use of individual purified gangliosides or mixtures of two gangliosides to restore cellular susceptibility to viral infection showed that GT1b and GQ1b were the most effective. The disialogangliosides were also active, principally GD1b, whereas GM1, GM3 were poorly active and GD3 inactive. Incubation of rabies virus with gangliosides prior to virus infection reduced the percentage of infected cells. The results indicate that highly sialylated gangliosides are part of the cellular membrane receptor structure for the attachment of infective rabies virus. However, it is possible that other glycoconjugates such as glycoproteins or glycolipids also participate as components of a receptor structure for rabies virus.
J Gen Virol 1986 Jan
PMID:Involvement of gangliosides in rabies virus infection. 286 68

Several species of small animals were inoculated at birth or as adults with blood components from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related disorders, or with the human immunodeficiency virus (HIV). No ill effects were noted in rats, hamsters, guinea-pigs, rabbits or musk shrews. Mice inoculated with clinical specimens had a significant incidence of mortality as compared with control groups (18.7% against 5.9%, P less than 0.025). Mice receiving HIV showed an increase in mortality, but it was not statistically significant. Infection of the animals by HIV could not be detected by virological or immunological studies. We concluded that none of these animal species provided a useful model for evaluating HIV infection.
J Gen Virol 1987 Aug
PMID:Small animals are not susceptible to human immunodeficiency virus infection. 288 49

Infection of mouse embryo fibroblasts in G1 or S phase with encephalomyocarditis virus gave different kinetics of viral RNA synthesis. In S phase cells, RNA synthesis was faster and reached higher levels than in G1 cells. Virus-specified proteins were fewer in G1 cells than in S cells during the early stage of the infection and c.p.e. in G1 cells appeared about 4 h later than in S cells. Addition of a cellular factor with ability to affect cell conformation had an inhibitory effect on viral RNA synthesis.
J Gen Virol 1985 Jul
PMID:Cell cycle position and expression of encephalomyocarditis virus in mouse embryo fibroblasts. 299 26

Somatic cell hybrids between rat XC(HPRT-) cells, non-permissive for herpes simplex virus type 1 (HSV-1) infection, and permissive mouse L(TK-) cells were constructed and karyotyped. Infection of these hybrid cells by HSV-1 strains F and MP revealed that they were susceptible to the virus. The amounts of virus produced by the hybrid cells, as well as the cytopathic effect observed, was very similar to that of the parental L(TK-) cells. Our results suggest that failure of HSV-1 to replicate in XC cells is more likely to be due to the absence of cellular elements required for efficient virus multiplication rather than to the presence of blocking or inhibiting factors.
J Gen Virol 1985 Aug
PMID:Susceptibility to herpes simplex virus type 1 infection of non-permissive rat XC(HPRT-) x permissive mouse L(TK-) hybrid cells. 299 44

Infection of NMRI mice with increasing doses of six different strains of herpes simplex virus type 1 (HSV-1) induced increasing levels of neutralizing antibodies. In contrast, three strains of HSV-2, irrespective of the dose, induced only marginal antibody responses. Only strain HG 52 (HSV-2) at high doses of infection stimulated antibody formation. The virus content of some organs in 6- to 8-week-old mice appeared to be lower after HSV-2 than after HSV-1 infection. Application of immune-modulating drugs [silica or poly(I) X poly(C) coupled via L-lysine to CM-cellulose] resulted in little augmentation of antibody formation if compared to HSV-1 infection. Secondary infections with HSV-1 or HSV-2 after a primary dose of HSV-1 were followed by a marked booster response. In contrast, a primary infection with HSV-2 suppressed secondary responses of HSV-1 and HSV-2, thus indicating fundamental differences between the antibody-stimulating potency of HSV-1 and HSV-2 strains.
J Gen Virol 1985 Oct
PMID:Differences in humoral immunogenicity between herpes simplex virus types 1 and 2. 299 56


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