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Biomedical subjects

H R Thacore

Publications and source records attributed to H R Thacore.

At least 37 records · Page 2Linked to original sources
PubMed1985

Characterization of lymphocyte interferons with different species specificities from normal and genetically dystrophic chickens.

Lymphocytes from thymus and spleen of normal (Line 412) and genetically dystrophic (Line 413) chickens produce two types of interferons (IFNs) with different host cell specificities. The first type, referred to as ChIFN-alpha, demonstrates antiviral activity on primary normal chicken embryo (CE) cells. This activity is stable at 60 degrees C for 1 h and, in this respect, ChIFN-alpha is similar to the standard ChIFN-beta. In contrast, the second type, referred to as ChIFN-alpha 1, demonstrates antiviral activity in human and simian cells but not in primary CE cells. This activity is labile at 60 degrees C for 1 h. The amount of these two types of IFNs produced in lymphocytes from the spleen of dystrophic chickens was fourfold greater than that produced from normal chickens under similar experimental conditions. In contrast to the lymphocytes from thymus and spleen, the lymphocytes from the bursa of both the normal and dystrophic chickens produced only one type of IFN, namely ChIFN-alpha 1. The development of antiviral state in human cells by ChIFN-alpha 1 requires host RNA synthesis. Although ChIFN-alpha 1 has antiviral properties similar to HuIFN-alpha in human cells, the two IFNs are not antigenically related.

Animals↗
PubMed1982

Interferon system of human cornea cells: interferon production, characterization, and development of antiviral state.

The interferon (IFN) system of human cornea cells in culture was studied. IFN produced by these cells by infection with Newcastle disease virus (NDV) was shown, by neutralization studies with specific antisera against human alpha interferon (HuIFN-alpha) and human beta interferon (HuIFN-beta), to contain 90-95% antiviral activity characteristic of the HuIFN-beta and 5-10% that of HuIFN-alpha. The chromatographic behavior of human cornea IFN on Con A-Sepharose and zinc chelate agarose columns was identical to that of HuIFN-beta produced by human foreskin cells. The cornea cells developed marked resistance when exposed to either HuIFN-beta or human gamma interferon (HuIFN-gamma) against vesicular stomatitis virus (VSV), but to a much lesser degree against HSV-1. Both the laboratory-adapted strain and a clinical isolate of HSV-1 were found to be resistant to HuIFN-beta and HuIFN-gamma as compared with VSV. The clinical isolate of HSV-1 was, however, more sensitive to HuIFN-gamma than the laboratory-adapted strain. Furthermore, a combination of HuIFN-beta and HuIFN-gamma did not significantly increase the level of antiviral state induced in cornea cells against HSV-1. These results suggest that in-vitro culture of human cornea cells can be a valuable system to evaluate the potential of chemotherapeutic agents against common ophthalmic viral infections.

Cells, Cultured↗
PubMed1981

Host restriction property of a vesicular stomatitis virus mutant isolated from carrier cultures.

Carrier cultures of L cells infected with wild-type vesicular stomatitis virus (VSV0) were initiated without the use of defective-interfering particles or homologous interferon. The cloned viruses recovered from such carrier cultures after passage 21 were characterized as temperature-sensitive. Furthermore, these clones of the mutant showed restricted replication at permissive temperature in HEp-2 cell cultures as compared to the wild-type VSV0. This restrictive replication of the mutant in HEp-2 cells was not due to a defect in the expression of virion-associated primary transcriptase activity in vivo, but due to the marked reduction in virus-specific characterized may govern the synthesis of mutant virus-specific amplified RNA in HEp-2 cells.

L Cells↗
PubMed1980

A sensitive method for quantification of vesicular stomatitis virus defective interfering particles: focus forming assay.

A focus-forming assay for the quantification of defective interfering (DI) particles of vesicular stomatitis virus (VSV) is described. This assay is based on the procedures described for lymphocytic choriomeningitis (LCM) virus by Popescu et al. (1976). Under appropriate conditions this focus-forming assay can quantify fewer than 100 DI particles/ml in a preparation containing a large number of infectious particles.

Animals↗
PubMed1978

Effect of interferon on transcription and translation of vesicular stomatitis virus in human and simian cell cultures.

The effect of interferons on vesicular stomatitis virus (VSV) primary transcription, amplified RNA synthesis [i.e. the sum of primary transcription RNA replication (leading to [ - ] RNA) and secondary transcription (leading to [ + ] RNA) and virus protein synthesis were studied. In a human cell line, both human and simian interferons inhibited the initiation of primary transcription and amplified RNA synthesis. In contrast, in a simian cell line tested similarly, the initiation of these activities was not affected, though they decreased as the infection progressed. Nevertheless, virus protein synthesis was completely inhibited. These results demonstrate that the action of interferon on virus transcription and/or translation may depend more on the host cell than on the particular interferon used.

Animals↗
PubMed1976

Rescue of vesicular stomatitis virus from homologous and heterologous interferon-induced resistance in human cell cultures by poxviruses.

In human cell cultures the ability of poxviruses to rescue vesicular stomatitis virus from human interferon-induced resistance was significantly more efficient than the ability to rescue it from simian interferon-induced resistance. The sensitivity of the poxvirus to interferon was not related to its ability to rescue vesicular stomatitis virus.

Animals↗
PubMed1975

Abortive infection of a rabbit cornea cell line by vesicular stomatitis virus: conversion to productive infection by superinfection with vaccinia virus.

An abortive infection of a rabbit cornea cell line (RC-60) by vesicular stomatitis virus (VSV), yielding less than 1 PFU/cell, was converted to a productive infection, yielding 1,900 PFU/cell, when cells were superinfected with vaccinia. Studies on the synthesis of VSV-directed RNA in RC-60 cells suggest that the abortive infection by VSV alone may be due in part to (i) a limited production of 40S virion RNA and (ii) a markedly reduced activity of virion-bound transcriptase activity in RC-60 cells compared to the activity in mouse L cells, a permissive host for VSV. No recognizable VSV structures, except a small amount of viral core structures, were produced by the abortive infection. In contrast, double infection of RC-60 cells with VSV and vaccinia in the presence of hydroxyurea resulted in the production of infective B particles of VSV. Although the function supplied by vaccinia responsible for the productive replication of VSV in double infected RC-60 cells has not been identified, metabolic inhibitor studies indicate that continuous vaccinia-dependent RNA synthesis is required for maximal production of infective VSV. The possibility is considered that vaccinia may supply a product or function required for VSV replication which is ordinarily supplied by the host but which is lacking in RC-60 cells.

Animals↗
PubMed1975

Infective and noninfective hemagglutinating particles of Newcastle disease virus: biological and chemical characterization.

Newcastle disease virus (Herts strain), grown in embryonated eggs or in a line of bovine kidney cells, was purified and then separated by sucrose density gradient centrifugation into infectious (IH) and noninfectious hemagglutinating (NIH) particles. These particles were morphologically similar, although the average size of IH was twice that of NIH particles. The activity of hemagglutinin per milligram of virus protein was two- to threefold higher in NIH particles than in IH particles, whereas the specific activity of neuraminidase did not differ in the two particle types. This was consistent with the observed particle size difference. The distribution of the major proteins in IH and NIH particles from egg-grown virus, determined by polyacrylamide gel electrophoresis (PAGE), was significantly different. In IH particles the molar ratio of protein 1 (74,000 daltons) to proteins 2 and 3 (56,000 daltons): protein 6 (41,000 daltons) was 1.0:2.5:2.5; in NIH particles the ratio was 1.0:0.6:1.0. When Newcastle disease virus was grown in bovine kidney cells, the molar ratio of proteins in IH particles resembled that of of egg-grown virus. However, in NIH particles from bovine kidney cells, only protein bands corresponding to protein 1 and proteins 2-3 were present and their molar ratio was 1.0:0.6. Protein 6 was marginally detectable in these particles. Analysis of the proteins in [3H]isoleucine- and [14C]glucosamine-labeled virus showed proteins 1 and 2 (glycoproteins) present in the ratio of 1.0:0.5; protein 3, the nucleoprotein, was not detected. These results are compatible with previous findings by others that NIH particles are deficient in RNA and nucleoprotein antigen, and suggest that formation of discrete particles of Newcastle disease virus by budding requires at most minimal amounts of proteins 3 or 6. The fatty acid composition of egg-grown IH and NIH particles was not significantly different and resembled that of normal allantoic fluid.

Cell Line↗
PubMed1973

Different sensitivity of ribonucleic and deoxyribonucleic acid viruses to resistance induced in rabbit cells (RK-13) by polyriboinosinic acid-polyribocytidilic acid.

When a continuous line of rabbit kidney cells (RK-13) was exposed to polyriboinosinic acid polyribocytidilic acid [poly(rI).poly(rC)], the cells became resistant to the replication of a ribonucleic acid (RNA) virus, vesicular stomatitis (VSV), but remained susceptible to the replication of two deoxyribonucleic acid (DNA) viruses, pseudorabies and vaccinia. These differences were identical to previous findings with RK-13 cells pretreated with exogenous rabbit interferon. Confirmation is thereby provided that RK-13 cells are deficient in the synthesis of resistance factors active against the DNA viruses tested and that there are separate resistance factors for RNA and DNA viruses in RK-13 cells. The resistance against VSV which developed in RK-13 cells exposed to poly(rI).poly(rC) could be significantly reversed by prior infection with infective vaccinia virus but not by vaccinia inactivated by ultraviolet irradiation or heat.

Animals↗
PubMed1972

Sensitivity of ribonucleic acid and deoxyribonucleic acid viruses to different species of interferon in cell cultures.

Although two deoxyribonucleic acid (DNA) viruses, pseudorabies (PsRV) and vaccinia, are as susceptible as a ribonucleic acid (RNA) virus, vesicular stomatitis (VSV), to interferon when tested in chicken or mouse cells, they are refractory to inhibition in interferon-treated primary rabbit kidney cells and in a continuous line (RK-13) of rabbit kidney cells. Superinfection with VSV of RK-13 cells first infected with PsRV completely blocks the replication of PsRV with no effect on VSV yield. When the same experiment is carried out in RK-13 cells pretreated with 1,000 units of interferon, VSV replication is inhibited, which permits PsRV to replicate normally. These findings demonstrate that in the same cell one virus (PsRV) can be refractory to interferon and a second virus (VSV) can be susceptible. These experiments show that rabbit kidney cell cultures are deficient in the synthesis of resistance factors active against the DNA viruses tested and raise the possibility that separate resistance factors may exist for RNA and DNA viruses. In the case of sequential infection of interferon-treated RK-13 cells with vaccinia and VSV, it was found that not only was vaccinia replication refractory to inhibition by interferon, but also that prior infection with vaccinia was able to partially reverse the effect of the inhibitor on the replication of the VSV used for superinfection. On the basis of these and other data it is postulated that a vaccinia virion component or a replication product of vaccinia virus, or both, enables VSV to escape the inhibiting action of interferoninduced resistance factors.

Animals↗
PubMed1972

Viral ribonuclei acid synthesis by Newcastle disease virus mutants isolated from persistently infected L cells: effect of interferon.

The synthesis of different viral ribonucleic acid (RNA) species was studied in chick embryo (CE) and mouse L-cell cultures infected with the Herts strain of Newcastle disease virus (NDV(o)) and a mutant isolated from persistently infected L cells (NDV(pi)). In CE cell cultures, both viruses synthesized significant amounts of 54, 36, and 18S RNA. However, in L cells, synthesis of 54S virion RNA was markedly reduced. From these results, it seems likely that the low yield of infective virus in L cells is due to a deficient synthesis of 54S RNA in this host. On this basis, however, it is apparent that the "covert" replication of NDV(o) in L cells is due to factors other than viral RNA synthesis. When low concentrations of interferon were used to pretreat CE cells, a differential effect on the synthesis of various RNA species was observed. The 18S RNA of NDV(o) was more sensitive to interferon action than the 36 and the 54S RNA species. In contrast, the 18S RNA of NDV(pi) was less sensitive than the 36S and the 54S RNA. The inhibition of 54S RNA synthesis correlated with the reduction of viral yield and explained the greater sensitivity of NDV(pi) to interferon.

Animals↗
PubMed1971

Cells persistently infected with Newcastle disease virus. 3. Thermal stability of hemagglutinin and neuraminidase of a mutant isolated from persistently infected L cells.

Data were obtained which indicated the possible cause of the defective elution from erythrocytes of the mutant virus (NDV(pi)) isolated from L cells persistently infected with the Herts strain of Newcastle disease virus (NDV(o)). The chicken erythrocyte receptors for the mutant and wild-type viruses were equally sensitive to the action of Vibrio cholera filtrate neuraminidase; this suggests that the failure of NDV(pi) to elute from chicken erythrocytes is not due to a specific neuraminidase-resistant receptor for this virus on the erythrocyte membrane. There was no difference in the enzyme content of the intact virions of NDV(o) and NDV(pi) when tested with a soluble substrate, indicating that the inefficient elution of NDV(pi) was not due to a reduced enzyme content. The neuraminidase activity of intact NDV(pi) virions was significantly more stable at 55 C than the enzyme of NDV(o) virions, whereas the dissociated enzymes of the two viruses were inactivated at the same rate. On the basis of these findings, it seems likely there is a structural difference between the two viruses. The neuraminidase protein of the mutant NDV(pi) may be incorporated into the viral envelope in such a manner that it is prevented from reacting with the substrate in the erythrocyte membrane, although it can react with a soluble substrate. The hemagglutinin activity of both intact and disrupted NDV(pi) was significantly more resistant to thermal inactivation than that of the wild-type NDV(o). This finding suggests a genetic difference in the hemagglutinin protein of the two viruses.

Animals↗