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At least 325 records · Page 18Linked to original sources

Microneutralization test in PK(15) cells for assay of antibodies to louping ill virus.

A microneutralization test in PK(15) cells was developed to measure the neutralizing antibody response of a group of ponies experimentally challenged with louping ill virus. Viral cytopathic effect was maximal after 6 days of incubation, at which point titration endpoints were clear-cut and readily determinable. The assay compared favorably with the mouse neutralization test for accuracy and ease of performance.

Animals↗

LYSOSOMAL ENZYMES IN CELLS INFECTED WITH CYTOPATHIC AND NON-CYTOPATHIC VIRUSES.

In chick embryo cells infected with fowl plague virus, an avian strain of influenza A which produces cytopathic effects, lysosomal enzymes were released from the particulate to the supernatant fraction of homogenates within 6 hours of infection. This change occurred in the presence of high concentrations of parafluorophenylalanine, suggesting that the changes were due to redistribution of preformed enzymes rather than to de novo protein synthesis. No such changes were observed when the Melbourne strain of influenza A virus multiplied in the same cell system without cytopathic effects. The possible role of lysosomal enzymes in virus uncoating and in the genesis of cytopathic effects is discussed.

Acid Phosphatase↗

The effect of phosphonoacetic acid on the in vitro replication of varicella-zoster virus.

Phosphonoacetic acid (PAA) was found to inhibit in vitro varicella-zoster virus (VZV) replication. At 100 microng/ml, PAA blocked the development and spread of VZV cytopathology in both growing and contact-inhibited cultures. Formation of virus plaques by infected cells and cell-free virus was effectively blocked at concentrations as low as 25 microng/ml. The development of nuclear and cytoplasmic virus antigens was also inhibited by PAA. Inhibition by PAA suggests that VZV DNA replication, like that of other herpes-viruses, involves a virus-specific DNA polymerase.

Acetates↗

Infectivity titration of the fast-replicating and cytopathic hepatitis A virus strain HM175A.2 by an in situ enzyme immunoassay.

A simple, rapid and objective infectivity assay based on an in situ enzyme immunoassay (EIA) was developed for the fast-growing and cytopathic cell culture-adapted hepatitis A virus (HAV) strain HM175A.2. Infectivity titration by EIA correlated well with titration by cytopathic effects. The reliability of this assay was demonstrated by close agreement in virus infectivity titers among different assays of the same virus aliquot and between assays of different virus aliquots. HAV infected cell cultures after fixation could be stored for up to 1 week before testing without decline in virus titer.

Antigens, Viral↗

Antiviral therapy.

The current status of antiviral therapy is reviewed, including discussion of older approaches together with more recently developed chemotherapy. Following the introduction dealing with pathophysiological aspects of virus disease, the different approaches to antiviral therapy are presented. The reasons for the slow progress in antiviral therapy are discussed. These include: 1. the necessity of intracellular penetration of drugs acting on viral replication; 2. the severe toxicity of most antiviral drugs; 3. the narrow antiviral spectrum of most of these agents; 4. the difficulty of making a rapid etiological diagnosis in view of the necessity of starting (specific?) treatment early in the course of the disease; 5. the difficult evaluation of beneficial as compared with deleterious effects of antiviral therapy. After a detailed review of clinically tested substances, including immunoglobulins, synthetic antiviral drugs (amantadine, nucleoside analogs, thiosemicarbazones and photodynamic dyes) and interferon, a guide concerning indications and application of specific antiviral therapy is presented. Although at present there are few indications, clinicians should be aware of the (present and future) possibilities of antiviral therapy.

Antibodies, Viral↗

LOCATION AND REGENERATION OF ENTERIOVIRUS RECEPTORS OF HELA CELLS.

Zajac, Ihor (Hahnemann Medical College, Philadelphia, Pa.), and Richard L. Crowell. Location and regeneration of enterovirus receptors of HeLa cells. J. Bacteriol. 89:1097-1100. 1965.-Treatment of live HeLa cells with chymotrypsin or trypsin completely inactivated the viral receptors for coxsackievirus B3 and poliovirus T1, respectively. Enzyme-treated cells regained their enterovirus receptor activity after incubation in culture medium. The existence of intracellular receptors for virus could not be demonstrated when live HeLa cells were treated with enzyme prior to disruption and fractionation. These results suggested that receptors for enteroviruses are limited to the cell surface.

Chymotrypsin↗

Immune response to respiratory syncytial virus: prevention of syncytia formation by human serum during in vitro infection.

Human serum specimens containing respiratory syncytial virus (RSV)-specific neutralizing antibody were found to prevent the formation of syncytia when applied to HEp-2 tissue culture monolayers which had been infected with RSV 12 h previously. This was evidenced by the demonstration of RSV-infected cells without any syncytia formation in the monolayers treated with RSV antibody-positive serum. On the other hand, widespread syncytia formation was observed with antibody-negative control serum. The inhibitory effects of RSV antibody progressively declined when applied beyond 12 h after infection. Protection of the monolayer against syncytia formation occurred only in the presence of antibody and was quickly lost after the serum was removed. The titer of antisyncytial antibody correlated with the titer of neutralization antibody.

Adult↗

Mouse hepatitis virus type 4 infection of primary glial cultures from genetically susceptible and resistant mice.

Mouse hepatitis virus type 4 infection of primary glial cultures, which consisted principally of astrocytes (marked by glial fibrillary acidic protein) from encephalitis-susceptible BALB/c or F1 (BALB/c x SJL/J) hybrid mice and resistant SJL/J mice, was studied. Primary neuron cultures from BALB/c and F1 hybrid mice were previously shown to be permissive and were destroyed within 5 days by infection with mouse hepatitis virus type 4, whereas neurons from SJL/J mice were fully resistant. In contrast, in the present study a chronic infection was established and maintained for up to 18 days in glial cultures from all three mouse strains. Infected SJL/J mouse glial cultures produced 10- to 50-fold less infectious virus and showed less cytopathic effect than did cultures from either infected BALB/c or F1 hybrid mice. Cytopathic effect was evident initially in cells from all three strains, and continued virus production occurred in the presence of limited additional cytopathic effect. These results were not due to the production of detectable levels of interferon. This study showed that SJL/J mouse primary glial cultures were permissive for mouse hepatitis virus type 4 infection whereas SJL/J primary neuron cultures were not, and that there was an early lytic phase of infection followed by chronic infection in all three strains.

Animals↗

Importance of antibodies to the fusion glycoprotein of paramyxoviruses in the prevention of spread of infection.

The effects of monospecific antibodies to the viral glycoprotein with hemagglutinating and neuraminidase activity (HN) and the viral glycoprotein with membrane-fusing activity (F) of the paramyxovirus simian virus 5 (SV5) on the spread of infection in two cell types have been investigated. In CV-1 cells, infection can spread by either released progeny virus adsorbing to and infecting other cells, or by fusion of an infected cell with an adjacent cell as a result of the cell-fusing activity of the F glycoprotein. In these cells, antibodies specific for the HN glycoprotein prevented the dissemination of infection by released infectious virus, but spread by cell fusion was not inhibited. Antibodies to the F glycoprotein completely prevented the spread of infection in these cells. In Madin-Darby bovine kidney cells, which are relatively resistant to SV5-induced fusion, antibodies to either the HN or F glycoproteins were capable of preventing the dissemination of infection. These results indicate that effective immunological prevention of the spread of paramyxovirus infection requires the presence of antibodies that inactivate the F glycoprotein. This requirement for anti-F antibodies has obvious implications for the design of effective paramyxovirus vaccines and provides an explanation for previous failures of formalin-inactivated paramyxovirus vaccines as well as additional insight into the possible immunopathological mechanisms involved in the atypical and severe infections that have occurred in individuals who received inactivated paramyxovirus vaccines and were subsequently infected by the virus.

Animals↗

BI-RG-587 is active against zidovudine-resistant human immunodeficiency virus type 1 and synergistic with zidovudine.

A series of dipyridodiazepinones have been shown to be potent inhibitors of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase. The lead compound, BI-RG-587, had a 50% inhibitory concentration of 84 nM against HIV-1 reverse transcriptase activity. This compound reduced plaque formation of HIV-1 in HeLa cells expressing the CD4 receptor by 50% at 15 nM. BI-RG-587 at comparable concentrations inhibited the production of p24 antigen following the acute infection of CEM T-lymphoblastoid cells or primary human monocyte-derived macrophages with HIV-1. No inhibitory effects against HIV-2 or against three picornaviruses were detected. Zidovudine (3'-azido-3'-deoxythymidine [AZT])-susceptible and AZT-resistant isolates of HIV-1 were equally susceptible to BI-RG-587. AZT and BI-RG-587 exhibited synergistic inhibition of HIV-1BRU at all concentrations examined.

Antigens, Viral↗

Isolation and assay of rabies serogroup viruses in CER cells.

Infection of CER cell cultures with field strains of rabies virus, ranging from 0 to 5 mouse brain passages, was detected by immunoflurescence within 2-4 days after infection. A fluorescent focus assay for measuring infectivity of seven rabies serogroup viruses was rapid and reproducible. Rabies field strians and other rabies serogroup viruses also induced cytopathic effect, usually on initial passage. The hemadsorption-negative (HAD-) plaque test in BSC-1 cells was successfully applied to laboratory-adapted rabies strains. HAD- test attempts were unsuccessful with CER cells and with field isolates of rabies virus in both cell lines. CER cells are heteroploid and are antigenically related to BHK-21 cells by fluorsecent antibody tests.

Antigens, Viral↗