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At least 1,441 records · Page 80Linked to original sources
PubMed1991

Coronavirus infection in the laboratory rat: immunization trials using attenuated virus replicated in L-2 cells.

Sixty-nine specific pathogen-free male Wistar rats approximately eight weeks of age were used to evaluate the efficacy of an attentuated strain of sialodacryoadenitis (SDA) virus in providing protection against infection on subsequent challenge with virulent SDA virus. Fifty-four animals were inoculated intranasally with approximately 10(3.5) median cell culture infectious doses of the 25th passage of SDA virus in L-2 cells. Randomly-selected vaccinated animals were killed in order to evaluate the safety and efficacy of attenuated virus by histopathological examination of the salivary glands, lacrimal glands, and lower respiratory tract, and titration of sera for antibody to SDA virus. At three months and six months postvaccination (pv), animals were selected at random and challenged with virulent SDA virus. Seronegative, age-matched animals were also challenged, and served as controls. In animals examined at six to ten days pv, lesions were absent in submandibular and parotid salivary glands and lacrimal glands, but transient lesions were present in major airways of the lower respiratory tract. In a comparison of the incidence and extent of lesions, and antibody titers in challenged vaccinates and seronegative controls, lesions were minimal or absent in vaccinates compared to challenged naive rats, particularly in animals inoculated at three months pv. In addition, antibody titers in challenged vaccinates were much higher than were postinoculation titers in inoculated controls. In a comparison of lesions in salivary and lacrimal glands in vaccinated and control animals challenged at six months pv, there was a significant reduction in the number of animals without lesions in the vaccinated group (p = less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

The UL4 gene of pseudorabies virus encodes a minor infected-cell protein that is dispensable for virus replication.

Although homologues of the open reading frame (ORF) UL4 of herpes simplex virus 1 (Human herpesvirus 1) have been found in the genomes of all hitherto-analysed alphaherpesviruses, little is known about their function. In a project to analyse systematically, in an isogenic and standardized assay system, the gene products of the alphaherpesvirus pseudorabies virus (PrV; Suid herpesvirus 1), the PrV UL4 gene product was identified using a monospecific rabbit antiserum prepared against a bacterial fusion protein. Western blot and immunofluorescence analyses revealed that the 146 codon UL4 ORF of PrV was translated into a nuclear 15 kDa protein which was detectable from 6 h after infection of rabbit kidney cells, but was not found in purified virus particles. For functional analysis, a UL4-negative virus recombinant (PrV-DeltaUL4F) was generated by mutagenesis of an infectious full-length clone of the PrV genome in E. coli. PrV-DeltaUL4F was replication-competent in rabbit kidney cells, and plaque formation was not affected by the mutation. However, maximum virus titres of PrV-DeltaUL4F were decreased about fivefold compared with wild-type PrV, and electron microscopy of infected cells demonstrated an impairment of release of mature virions. This growth defect of PrV-DeltaUL4F could be corrected completely by propagation in UL4-expressing cells. Correlating with the inconspicuous in vitro phenotype, neurovirulence of PrV-DeltaUL4F was also not affected significantly. Thus, UL4 encodes a non-structural protein of PrV that enhances virion formation but is not essential for PrV replication in vitro or in vivo.

Animals↗
PubMed1978

Enhanced virus replication in mammalian cells exposed to commercial emulsifiers.

Mammalian cell cultures were used to show that a variety of commercial emulsifiers are capable of enhancing the sensitivity of these cells to infection with several viruses. Some emulsifiers were not active as enhancers, and those viruses that responded to the enhancing emulsifiers were single-stranded ribonucldic acid viruses. The double-stranded viruses that were tested were nonresponders.

Cell Line↗
PubMed1986

Inhibition of vaccinia virus replication in RK-13 cells by N,N'-bis(methylisatin-beta-thiosemicarbazone)-2-methylpiperazine.

N,N'-bis(methylisatin-beta-thiosemicarbazone)-2-methylpiperazine in a 100 mumol/l concentration inhibited the reproduction of vaccinia virus in RK-13 cells by about 90%. This compound (bis-IBTMP) had no influence on virus adsorption and on early stages of virus multiplication, but affected virus reproduction from 12 to 24 hr post-infection (p.i.). The incorporation of 3H-thymidine into infected cells increased during first 10 hr p.i., decreasing gradually afterwards. In the infected cells treated with bis-IBTMP the same tendency was observed up to 10 hr p.i., but later on the incorporation level remained unchanged. The uptake of 14C-amino acids in the presence of bis-IBTMP was reduced both in vaccinia virus-infected and non-infected RK-13 cells.

Animals↗
PubMed1981

Enhancement of varicella-zoster virus replication in cultured human embryonic lung cells treated with the pesticide carbaryl.

In studies designed to determine the factors responsible for control of herpesvirus replicaton in an infected cell, we examined the interaction of varicella-zoster (VZ) virus-infected human embryonic lung cells with the pesticide carbaryl. The replication of the cell-associated VZ virus was enhanced 2- to 13-fold as compared to control cultures in Sevin 4 Oil-treated cultures and in cultures treated with the pesticide's active ingredient, carbaryl. The replication of VZ virus in cultures teated with the base oil plus inert ingredients found in the pesticide formulation was not enhanced. Possible differences in cytotoxicity induced by Seven 4 Oil, pure carbaryl, or the base oil preparation were ruled out since treated and control cultures were shown to have similar numbers of viable cells when measured by trypan blue exclusion tests or by the ability of treated cells to form foci. A dose response study showed a decrease in viral enhancement in cells treated with decreasing carbaryl concentrations.

Carbaryl↗
PubMed2004

Cytotoxic T lymphocyte-based control of simian immunodeficiency virus replication in a preclinical AIDS vaccine trial.

Recently, encouraging AIDS vaccine trials in macaques have implicated cytotoxic T lymphocytes (CTLs) in the control of the simian human immunodeficiency virus SHIV89.6P that induces acute CD4(+) T cell depletion. However, none of these vaccine regimens have been successful in the containment of replication of the pathogenic simian immunodeficiency viruses (SIVs) that induce chronic disease progression. Indeed, it has remained unclear if vaccine-induced CTL can control SIV replication. Here, we show evidence suggesting that vaccine-induced CTLs control SIVmac239 replication in rhesus macaques. Eight macaques vaccinated with DNA-prime/Gag-expressing Sendai virus vector boost were challenged intravenously with SIVmac239. Five of the vaccinees controlled viral replication and had undetectable plasma viremia after 5 wk of infection. CTLs from all of these five macaques rapidly selected for escape mutations in Gag, indicating that vaccine-induced CTLs successfully contained replication of the challenge virus. Interestingly, analysis of the escape variant selected in three vaccinees that share a major histocompatibility complex class I haplotype revealed that the escape variant virus was at a replicative disadvantage compared with SIVmac239. These findings suggested that the vaccine-induced CTLs had "crippled" the challenge virus. Our results indicate that vaccine induction of highly effective CTLs can result in the containment of replication of a highly pathogenic immunodeficiency virus.

AIDS Vaccines↗
PubMed1979

Cellular localization of Saint Louis encephalitis virus replication.

Replication of Saint Louis encephalitis (SLE) virus was inhibited when PS cells were treated with actinomycin D, daunomycin or cordycepin during the first 9 hr after infection. Autoradiography of SLE virus-infected pulse labelled cells demonstrated that viral RNA synthesis is localized within the nuclear area. Nuclei purified from cells after 12 hr of infection contained heterogeneous 20 S to 26 S viral RNA but no SLE virus genome sized 43 S RNA. Later during infection, nuclei isolated from infected cells contained large amounts of 43 S and 20 S to 26 S RNAs. The 43 S viral RNA present in cells late in infection could not be removed with 1% Tween 80: Nonidet P 40. Purified nuclei isolated from cells early in infection supported the synthesis of 43 S virion RNA in the absence of cytoplasmic factors. The cytoplasmic membrane fraction prepared from cells early in infection contained heterogeneous 10 S to 26 S RNA species; later during infection these membranes contained viral 43 S, 26 S to 30 S and 4 S RNA. These results suggest that the nucleus is an important site of early viral synthesis.

Animals↗