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At least 19 recordsLinked to original sources

Role of virus variants and cells in maintenance of persistent infection by measles virus.

Hamster embryo fibroblasts persistently infected with a derivative of the Schwarz vaccine strain of measles virus spontaneously released virus particles with an average buoyant density considerably lower than that of the parental virus. The released virus contained all of the measles virus structural proteins and interfered with replication of standard virus. All of the virus structural proteins were associated with a membrane-free cytoplasmic extract from the persistently infected cells. Membrane-free cytoplasmic extracts prepared from Vero cells lytically infected with Schwarz strain measles contained little or no virus envelope structural protein. Maintenance of persistent infection may involve both the presence of virus variants and a defect in the ability of the infected cell to replicate the virus efficiently.

Animals

Characterization of two Chikungunya virus variants.

The stability of virulence and plaque size of two variants of Chikungunya virus (genus Alphavirus) were examined. Mouse pathogenicity did not coincide with infective virus levels in the brain. An increase in the average survival times of mice receiving a lethal dose of the variant which allowed prolonged survival at high doses and harvested late after infection was observed. Studies in Vero cells suggested that the number of infective virus particles produced per cell was lower with the small plaque variant, though these cells were selective for this clone. On the other hand suckling mice or antisera favoured a more virulent large plaque variant.

Animals

Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression.

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.

Animals

Geographical distribution of swine (Hsw1N1) and Hong Kong (H3N2) influenza virus variants in pigs in Southeast Asia.

Influenza viruses of the Hsw1N1 and H3N2 subtypes were isolated in Hong Kong from pigs originating from Hong Kong, People's Republic of China (PRC), Singapore, and Taiwan. The H3N2 isolates were from pigs from Hong Kong and PRC, whereas the Hsw1N1 isolates were from pigs from Hong Kong, PRC, Singapore and Taiwan. The hemagglutinins of the H3N2 isolates were similar to those of the earlier A/Hong Kong/1/68 and A/Port Chalmers/1/73 variants from man. The Hsw1N1 isolates were similar to the human A/New Jersey/8/76 virus. These studies extend the geographical range of Hsw1N1 influenza virus and suggest that pigs in southeast Asia, like those in North America, harbor Hsw1N1 influenza viruses. These findings underline the importance of pigs as potential reservoirs for future human pandemics by the continued isolation (in Asia) of H3N2 and Hsw1N1 influenza viruses.

Animals

[Comparative antigenic characteristics of 2 Marek's disease virus variants and of herpesvirus of turkeys isolated in the USSR].

The antigens induced by pathogenic (55) and nonpathogenic (83) variants of Marek's disease virus, the Kekava strain (MDV-Kekava) and herpesvirus of turkeys, the M-24-72 strain (HVT-M24-72) were tested in the agar gel precipitation test. The antigens were prepared from feather follicles (FF) of the infected chickens, from the infected cultures of chick embryo fibroblasts (CEF) and from the culture fluid (CF) of these culttures. In the FF and CEF cultures infected with MDV-Kekava-83, the synthesis of the antigens was 6-10 times as low as in the FF and CEF cultures infected with MDV-Kekava-55. Both variants of MDV-Kekava retained their capacity for antigen synthesis in the CF up to 84 passages. Three antigens or three groups of antigens were found in the preparations examined: (1) strong common antigens in the CF and FF preparations; (2) weak common antigens in cell preparations and CF; (3) strong antigen(s) in cell preparations not identical to the CF and FF antigens. In CEF culture preparations infected with MDV-M-24-72, using sera from chickens with Marek's disease an antigen was detected partially identical to the weak antigen of cell preparations and cross-reacting with strong antigens of the FF, CF and cell antigens of MDV. No antigen was found in concentrates of CF from the CEF cultures infected with MDV-M-24-72 with the sera used. It is suggested that the CF and FF MDV antigens are virus antigens, while antigens of the cell preparations of this strain are autoantigens or embryonal antigens. Data are presented on relationship between the MDV-Kekava antigens with the MDV-HPRS-16 antigen.

Animals

The isolation of a Bwamba virus variant from man in Western Kenya.

A bwamba group virus was isolated from the blood of a febrile child on the Kano Plain, Kenya. The isolate (NY-45), closely resembling Bwamba, established infection in both Anopheles gambiae and Mansonia uniformis. Neither the Bwamba nor the Pongola prototype strains grew in both species. In gel-diffusion tests NY-45 virus passaged through mosquitoes exhibited a line of identity with Pongola antiserum. In contrast no cross-reaction was observed with NY-45 virus which had not previously been passaged through mosquitoes.

Adult

Recovery of a Sendai virus variant with temperature-sensitive hemolytic activity from persistently infected cells from mouse brain.

A persistently infected cell line designated MB/Senas was established by cultivation of mouse brain cells from four-day-old C3H mice infected intracerebrally at birth with 10(6) PFU of Sendai virus, strain 52. After 5 passages, 0.16 per cent of Sendai52 antiserum (containing two 50 per cent plaque reducing doses/ml of serum) was introduced into the culture medium. The addition of antiserum was accompanied by a rise in cell-associated viral antigen from a level of 5 per cent antigen positive cells to 100 per cent demonstrable by both intracellular and membrane immunofluorescence. A variant of Sendai52 virus, designated Sendaias, was recovered from MB/Senas by inoculation of supernatant medium into chick embryos. Infection of chick embryos at 37 degrees C was abortive. Fifty per cent or less of chick embryos infected at dilutions 10(-1) to 10(-9) yielded detectable virus. Hemagglutination (HA) was weak but could be improved by trypsinization of allantoic fluids. Neuraminidase (NA) activity was barely detectable. Hemolysis (HE) was absent. Propagation of Sendaias virus at 33 degrees C showed no change from weak HA and NA activities but HE activity was now apparent which was temperature sensitive. Mortality of infected chick embryos increased to 100 per cent. HE activity and lethality for chick embryos was thermolabile at 45 degrees C.

Cell Line

Selection of La Crosse virus variants by sentinel squirrels (Sciuris carolinensis) and chipmunks (Tamius striatus).

Comparisons of La Crosse (LAC) virus strains, obtained from sentinel squirrels and chipmunks, were made using three viral markers: plaque size on Vero cells, virulence in 8 days old laboratory mice, and antigenic characteristics as measured by the plaque reduction neutralization test. All strains were in their first suckling mouse brain passage. The mean plaque size of viruses isolated from squirrels was slightly larger than the mean plaque size of viruses isolated from chipmunks. There were no differences in virulence and antigenic characteristics of LAC strains isolated from chipmunks compared to those from squirrels. However, significant differences in these characteristics between individual virus strains did occur, irrespective of the vertebrate species from which the strain was isolated. First suckling mouse brain passage of viremic blood apparently selected for a smaller mean plaque size than was present in the blood. These results indicate that the squirrel and chipmunk were not rapidly selecting for greatly divergent subpopulations of the three measured markers in nature. There were some indications, however, that even one suckling mouse brain passage of field LAC virus apparently decreased mean plaque size.

Animals

Emergence of a Bundibugyo virus variant in the 2026 outbreak in the Democratic Republic of the Congo and Uganda.

In May 2026, an outbreak of Ebola disease caused by Bundibugyo virus (BDBV, species Orthoebolavirus bundibugyoense) was declared in the Democratic Republic of the Congo (DRC), with cases originating from DRC and locally transmitted cases reported in Uganda. Bundibugyo virus disease (BVD) outbreaks were previously recorded in 2007-2008 in Bundibugyo District, Uganda, and in 2012 in Isiro, DRC. Here, we generated 22 genomes from samples obtained from individuals with BVD in DRC and Uganda. These genomes form a well-supported phylogenetic cluster separate from BDBV variants associated with the 2007 and 2012 outbreaks, together with evidence for sustained human transmission. This is consistent with the emergence of a new zoonotic spillover event rather than resurgence from previously reported variants. Besides ongoing efforts in strengthening surveillance systems, community engagement, establishing Ebola treatment centers, and developing targeted medical countermeasures; our report advocates to specifically increase decentralized laboratory diagnostics capacity, with pan-Orthoebolavirus assays, including genomic sequencing capacity, for limiting further outbreak expansion, timely detection and control of future outbreaks.

Journal Article

Relationship in nucleic acid sequences between mouse mammary tumor virus variants.

Primary cultures of mouse mammary carcinomas were used as a source of both radioactively labeled and unlabeled 60-70S RNA of mouse mammary tumor virus (MMTV) obtained from various mouse strains. Competition molecular hybridization experiments revealed that, within the limits of the assay, the RNAs of the MMTVs synthesized in culture by the tumors of the mouse strains RIII, GR, A, and C3H, are identical. A comparison of the genomes of the milk-transmitted MMTV(C3H) and the vertically transmitted MMTV(C3Hf) revealed that these two viruses are approximately 75% similar. No nucleic acid sequence homology was observed between MMTV(C3H) 60-70S RNA and the RNAs of murine leukemia virus, Mason-Pfizer virus, or the BrdUrd-induced type-B quinea pig virus.

Animals

Host-interferon-stimulated gene response to virus-host recombinant variants of hepatitis E virus and enhanced viral replication.

The hepatitis E virus (HEV) is a leading cause of acute hepatitis worldwide. HEV infection can become chronic in immunocompromised individuals, in whom virus-host recombinant variants (VHRVs) can be detected. These variants often harbor host-derived insertions in the polyproline-rich region (PPR), and most display enhanced replication in vitro. However, the mechanisms underlying this replicative advantage remain unclear. It is likely that genes of the infected cells are differentially expressed according to the replicative capacity of the strain. The host factors involved in the improvement of the replicative capacity of these VHRVs are yet to be identified.In this study, we analyzed the host transcriptional response to seven VHRVs in HepG2/C3A cells using bulk RNA sequencing at 48 h and 168 h post-infection. Five VHRVs (RNF19A, ZNF787, KIF1B, RPS17, EEF1A1) previously associated with a high replication rate induced more significant, distinct transcriptomic changes than low-replicative variants (RNA18, RPL6), particularly at 168 h. A shared set of 25 genes, especially interferon-stimulated genes (ISGs), was upregulated in cells infected with high-replicating variants. Interestingly, ISG induction was limited at 48 h despite high viral RNA concentrations, suggesting a delayed antiviral response. At 168 h, high ISG expression coincided with high viral loads, indicating that VHRVs may evade or exploit immune defenses. Our findings reveal candidate ISGs such as IFIT1 and ISG15 that may influence HEV persistence and immune escape. These results offer new insights into the interplay between VHRV replication and host immunity.IMPORTANCEHepatitis E virus (HEV) is a major cause of acute hepatitis and can cause chronic infections in immunocompromised individuals. Virus-host recombinant variants (VHRVs) having integrated host-derived insertions often replicate more effectively, yet the host determinants of this phenotype remain unclear. With RNA sequencing of HepG2/C3A-infected cells, we observed that high-replicating VHRVs induce a delayed but strong expression of interferon-stimulated genes (ISGs), including IFIT1 and ISG15, despite high viral loads. These results suggest that VHRVs may transiently modulate or evade aspects of host antiviral defenses. Our study revealed host transcriptional patterns associated with enhanced viral replication, providing insight into potential mechanisms that enhance HEV replication and highlighting candidate pathways that could influence the interplay between viral replication and immune responses, all requiring further investigation.

Humans

Glucose tolerance and pancreatic ultrastructure in mice with long-term diabetes induced by EMC virus (M variant) (38518).

Of 27 young male CD-1 mice infected with the M variant of the encephalomycarditis (EMC) virus and surviving for 11 or 12 mo, all but three had normal glucose tolerance curves, and all displayed normal islet cell morphology, at the time of sacrifice, in spite of an initital hyperglycemic response. Three animals maintained diabetic glucose tolerance curves one year after infection but they, too, failed to show significant morphological alterations in their pancreatic beta cells.

Animals

Differentiation of the haemagglutinin genes of variant influenza viruses by RNA-RNA hybridization.

The genetic compositions of four antigenic variants of A/Memphis/1/71 (H3N2) influenza virus, which were selected by growth in the presence of monoclonal antibodies against the haemagglutinin, were compared. The results indicate that the mutant haemagglutinin genes can be differentiated by polyacrylamide gel electrophoresis of the double stranded RNA hybrids formed between virion RNA and transcripts isolated from infected cells.

Genes, Viral

In vitro comparison of foot-and-mouth disease virus subtype variants causing disease in vaccinated cattle.

Foot-and-mouth disease virus isolates of types O, A and SAT 2, from diseased animals in herds routinely vaccinated twice a year were compared antigenically with the vaccine strains in the complement-fixation, neutralization and radial immunodiffusion tests. It was found that strains which had readily infected vaccinated cattle had R values against the vaccine strain in the complementfixation and radial immunodiffusion tests of 30 or less, while strains causing primary outbreaks with little spread had R values of 30-40. Threefold differences in humoral neutralizing antibody concentration between the field variant and the vaccine strain in sera from vaccinated animals were likely to be significant in terms of protection.

Animals