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PubMed1988

Simian virus 40 revertant enhancers exhibit restricted host ranges for enhancer function.

We have assayed the cell-specific activity of a matched set of four enhancers found in viral revertants derived from simian virus 40 (SV40) enhancer mutants. These enhancers all contain 71-base-pair duplications that span identical regions or, in one case, the same region shifted by 2 nucleotides. The four enhancers differ, however, in that each one either carries a different wild-type pair of the genetically defined SV40 enhancer A, B, or C elements, with the other two elements mutated, or carries all three elements mutated. The three enhancers carrying two copies of a wild-type element effectively enhance transcription in CV-1 and HeLa cells, but only the enhancer containing a duplicated wild-type C element exhibits activity in NIH 3T3 cells. These results show that the ability of the A, B, and C elements to compensate for one another is cell specific and that selection for enhancer function in one cell type can generate enhancers with different cell-specific activities. These results are consistent with the hypothesis that tandem duplication of multiple distinct enhancer elements, as in wild-type strains of SV40 (e.g., the 72-base-pair repeat), has the property of expanding the host range of an enhancer.

Animals↗
PubMed1993

[Variation of influenza viruses and their recognition of the receptor sialo-sugar chains].

Influenza A, B viruses contain 2 viral specific, membrane associated glycoprotein antigens, hemagglutinin and sialidase. Hemagglutinin is essential for the initial binding of the virus to the cell membrane receptors that contain sialic acid such as gangliosides and sialo-glycoproteins. Hemagglutinin is also important for the intracellular viral uncoating by the low pH fusion processes. The evolution of the influenza viruses and host range variation come from the mutation of hemagglutinin and sialidase genes and change of their sialo-sugar chain recognition together with alteration in the antigenic epitopes. In this report, the molecular mechanism of the relationship between the evolutional change of the viral glycoproteins, especially hemagglutinin molecules and the change of the receptor binding specificity is reported, and also the strategy for the development of a new universal vaccine which generates the antibody whose supervariable region mimics the common receptor sialo-sugar chains for all the subtypes of influenza viruses is also described.

Amino Acid Sequence↗
PubMed1981

In vitro host range of equine infectious anemia virus.

Equine infectious anemia virus (EIAV) was successfully inoculated onto cell cultures of canine and feline origin, resulting in chronic infections in these cultures. Infection of equine cell cultures, which were the previous sole in vitro source demonstrated for virus production, was also performed for comparative purposes. Determination of the nature of the virus produced in the heterologous as well as the equine cells was accomplished in several ways. SDS-PAGE of purified virus from the different cell lines indicated very similar protein composition. Immunological identity was observed in gel diffusion tests employing an antiserum to the major core protein (p24) of equine-derived EIAV. Competition radioimmunoassays also indicated similar antigenicity in the viruses derived from the several cell lines. Strong relatedness was further demonstrated by hybridization of viral RNAs to EIAV complementary DNA. These data indicate that EIAV has an amphotropic cell culture host range and that the viruses isolated from the permissive lines were similar.

Animals↗
PubMed2001

A short N-proximal region in the large envelope protein harbors a determinant that contributes to the species specificity of human hepatitis B virus.

Infection by hepatitis B virus (HBV) is mainly restricted to humans. This species specificity is likely determined at the early phase of the viral life cycle. Since the envelope proteins are the first viral factors to interact with the cell, they represent attractive candidates for controlling the HBV host range. To investigate this assumption, we took advantage of the recent discovery of a second virus belonging to the primate Orthohepadnavirus genus, the woolly monkey HBV (WMHBV). A recombinant plasmid was constructed for the expression of all WMHBV envelope proteins. In additional constructs, N-terminal sequences of the WMHBV large envelope protein were substituted for their homologous HBV counterparts. All wild-type and chimeric WMHBV surface proteins were properly synthesized by transfected human hepatoma cells, and they were competent to replace the original HBV proteins for the production of complete viral particles. The resulting pseudotyped virions were evaluated for their infectious capacity on human hepatocytes in primary culture. Virions pseudotyped with wild-type WMHBV envelope proteins showed a significant loss of infectivity. By contrast, infectivity was completely restored when the first 30 residues of the large protein originated from HBV. Analysis of smaller substitutions within this domain limited the most important region to a stretch of only nine amino acids. Reciprocally, replacement of this motif by WMHBV residues in the context of the HBV L protein significantly reduced infectivity of HBV. Hence this short region of the L protein contributes to the host range of HBV.

Amino Acid Sequence↗
PubMed2026

H5N1 Clade 2.3.4.4b Infections in Domestic Cats During an Avian Influenza Outbreak in Italy: Implications for One Health Surveillance.

BACKGROUND: H5Nx goose/Guangdong (Gs/GD) lineage highly pathogenic avian influenza (HPAI) viruses pose a significant public health threat due to their global spread, mutation accumulation, and expanding host range. The descendant clade 2.3.4.4b has been causing widespread infections in birds and increasing spillover events in mammals. METHODS: This report documents the first fatal case of highly pathogenic avian influenza virus (HPAIV) H5N1 clade 2.3.4.4b infection in a domestic cat in Italy, detected in early January 2025. The cat (CAT 1) resided on a backyard poultry farm experiencing a high pathogenicity avian influenza outbreak and succumbed rapidly following the onset of respiratory signs. A second exposed cat (CAT 2) developed clinical disease without fatal outcome. Comprehensive outbreak investigations were conducted, including pathological, serological, molecular analyses, and genomic characterization. RESULTS: Pathological examination of CAT 1 revealed acute necrotizing bronchointerstitial pneumonia, non-suppurative meningoencephalitis, and disseminated foci of hepatic necrosis. Interestingly, the PB2-E627K mutation associated with mammalian virus adaptation was observed in the feline viral isolate compared to avian isolates. Such polymerase complex mutations are key determinants of host range and increase pathogenicity in mammals. CAT 2 from the same farm tested negative for AIV genome detection but subsequently seroconverted for antibodies against NPA, H5, and N1. CONCLUSION: Sharing these findings is crucial for surveillance aimed at enabling early identification of increased risks to human and animal health, preventing cross-species viral transmission and mitigating the risk of potential spillover events.

Animals↗
PubMed1976

Viral DNA-synthesizing intermediate complex isolated during assembly of bacteriophage phi X174.

A DNA protein complex that is a precursor of mature phi X174 phage was isolated. The complex sedimented with an S value of 50 in a sucrose gradient and contained phage DNA consisting of a replicative form molecule with an extended tail of single-stranded viral DNA. The viral-strand DNA ranged from one to two genomes in length. Proteins coded on the phi X174 genome as well as the host genome were associated with the viral DNA in the 50S precursor complex. Our results indicated that both viral DNA synthesis and cleavage of the growing viral-strand DNA occurred in the 50S complex.

Coliphages↗
PubMed2001

Identification and analysis of a new hepadnavirus in white storks.

We identified, cloned, and functionally characterized a new avian hepadnavirus infecting storks (STHBV). STHBV has the largest DNA genome of all avian hepadnaviruses and, based on sequence and phylogenetic analysis, is most closely related to, but distinct from, heron hepatitis B virus (HHBV). Unique for STHBV among the other avian hepadnaviruses is a potential HNF1 binding site in the preS promoter. In common only with HHBV, STHBV has a myristylation signal on the S and not the preS protein, two C terminally located glycosylation sites on the precore/core proteins and lacks the phosphorylation site essential for the transcriptional transactivation activity of duck-HBV preS protein. The cloned STHBV genomes were competent in gene expression, replication, and viral particle secretion. STHBV infected primary duck hepatocytes very inefficiently suggesting a restricted host range, similar to other hepadnaviruses. This discovery of stork infections unravels novel evolutionary aspects of hepadnaviruses and provides new opportunities for hepadnavirus research.

Amino Acid Sequence↗
PubMed1995

Virus and host-specific adaptations in the BL1 and BR1 genes of bipartite geminiviruses.

The host range of individual geminiviruses may be quite narrow, and closely related viruses can exhibit distinct host adaptations. Two such bipartite geminiviruses are bean golden mosaic virus (GBMV) and tomato golden mosaic virus (TGMV). In both, the BL1 and BR1 genes are required for the spread of virus infection in plants. We have investigated the contributions of BL1 and BR1 to host-specific phenotypes of BGMV and TGMV by constructing hybrid viruses in which these coding regions were exchanged. Hybrids were assayed on bean, a good host for BGMV, and Nicotiana benthamiana, a good host for TGMV. A BGMV hybrid having TGMV BL1 and BR1 efficiently infected beans, but elicited attenuated symptoms. In N. benthamiana, this hybrid had slightly increased virulence and DNA accumulation relative to wild-type BGMV. A TGMV hybrid having BGMV BL1 and BR1 was virulent in N. benthamiana, but elicited attenuated symptoms. However, this hybrid exhibited no gain of function in beans relative to wild-type TGMV. Hybrid viruses with TGMV BL1 and BGMV BR1 had severely defective phenotypes in either viral or host background. Although exchanging BL1 and BR1 between BGMV and TGMV did not change host range, some host adaptation of these genes is suggested. However, virus-specific compatibility between BL1 and BR1 is of more importance for viability. Thus, these gene products may act in concert to potentiate virus movement.

Adaptation, Physiological↗
PubMed2004

Infectivity analysis of two variable DNA B components of Mungbean yellow mosaic virus-Vigna in Vigna mungo and Vigna radiata.

Mungbean yellow mosaic virus-Vigna (MYMV-Vig), a Begomovirus that causes yellow mosaic disease, was cloned from field-infected blackgram (Vigna mungo). One DNA A clone (KA30) and five different DNA B clones (KA21, KA22, KA27, KA28 and KA34) were obtained. The sequence identity in the 150-nt common region (CR) between DNA A and DNA B was highest (95%) for KA22 DNA B and lowest (85.6%) for KA27 DNA B. The Rep-binding domain had three complete 11-nt (5'-TGTATCGGTGT-3') iterons in KA22 DNA B (and KA21, KA28 and KA34), while the first iteron in KA27 DNA B (5'-ATCGGTGT-3') had a 3-nt deletion. KA27 DNA B, which exhibited 93.9% CR sequence identity to the mungbean-infecting MYMV, also shared the 3-nt deletion in the first iteron besides having an 18-nt insertion between the third iteron and the conserved nonanucleotide. MYMV was found to be closely related to KA27 DNA B in amino acid sequence identity of BV1 (94.1%) and BC1 (97.6%) proteins and in the organization of nuclear localization signal (NLS), nuclear export signal (NES) and phosphorylation sites. Agroinoculation of blackgram (V. mungo) and mungbean (V. radiata) with partial dimers of KA27 and KA22 DNA Bs along with DNA A caused distinctly different symptoms. KA22 DNA B caused more intense yellow mosaic symptoms with high viral DNA titre in blackgram. In contrast, KA27 DNA B caused more intense yellow mosaic symptoms with high viral DNA titre in mungbean. Thus, DNA B of MYMVVig is an important determinant of host-range between V. mungo and V. radiata.

Amino Acid Motifs↗
PubMed1997

[Host range of influenza viruses and their receptor binding specificities].

Host-range of influenza viruses are established by many factors in nature such as the quantitative, qualitative aspects of the viral receptor, the permissive and non permissive states of host-cell condition, and also the antibody and inhibitor pressure present in the host. Influenza virus hemagglutinin recognizes specific sialyl-sugar chains of the host cell membranes. In this paper, the structure and function of sialyl-sugar chains as influenza virus receptors are described in relation to the variation of influenza viruses and the molecular evolution of influenza virus hemagglutinin.

Hemagglutinin Glycoproteins, Influenza Virus↗
PubMed1997

The range and distribution of murine central nervous system cells infected with the gamma(1)34.5- mutant of herpes simplex virus 1.

Wild-type herpes simplex virus 1 (HSV-1) multiplies, spreads, and rapidly destroys cells of the murine central nervous system (CNS). In contrast, mutants lacking both copies of the gamma(1)34.5- gene have been shown to be virtually lacking in virulence even after direct inoculation of high-titered virus into the CNS of susceptible mice (J. Chou, E. R. Kern, R. J. Whitley, and B. Roizman, Science 250:1262-1266, 1990). To investigate the host range and distribution of infected cells in the CNS of mice, 4- to 5-week-old mice were inoculated stereotaxically into the caudate/putamen with 3 x 10(5) PFU of the gamma(1)34.5- virus R3616. Four-micrometer-thick sections of mouse brains removed on day 3, 5, or 7 after infection were reacted with a polyclonal antibody directed primarily to structural proteins of the virus and with antibodies specific for neurons, astrocytes, or oligodendrocytes. This report shows the following: (i) most of the tissue damage caused by R3616 was at the site of injection, (ii) the virus spread by retrograde transport from the site of infection to neuronal cell nuclei at distant sites and to ependymal cells by cerebrospinal fluid, (iii) the virus infected neurons, astrocytes, oligodendrocytes, and ependymal cells and hence did not discriminate among CNS cells, (iv) viral replication in some neurons could be deduced from the observation of infected astrocytes and oligodendrocytes at distant sites, and (v) infected cells were being efficiently cleared from the nervous system by day 7 after infection. We conclude that the gamma(1)34.5- attenuation phenotype is reflected in a gross reduction in the ability of the virus to replicate and spread from cell to cell and is not due to a restricted host range. The block in viral replication appears to be a late event in viral replication.

Animals↗
PubMed1988

Avian reovirus mRNAs are nonfunctional in infected mouse cells: translational basis for virus host-range restriction.

Avian reovirus S1133 penetrates and uncoats in suspension cultures of mouse L cells. The multiple species of viral transcripts are produced in the cytoplasm of the infected cell, but they fail to associate with polysomes, consistent with the absence of viral protein synthesis. The selective block in avian virus mRNA translation is not overcome by coinfection with mammalian reovirus type 3, which replicates in mouse L cells, or by hypertonic shock or exposure to a low concentration of cycloheximide. Although the avian viral transcripts are inactive in vivo, RNA extracted from infected, nonpermissive L cells directs the synthesis of a normal spectrum of viral proteins in rabbit reticulocyte lysates. These results indicate that avian viral transcription is not restricted in mouse cells and that viral replication is prevented at the level of initiation of protein synthesis.

Animals↗
PubMed1974

A distinct class of inducible murine type-C viruses that replicates in the rabbit SIRC cell line.

The existence of the selectively permissive rabbit cell line SIRC allows definition of a new class of endogenous murine type-C virus. Continuous clonal lines of transformed cells derived from the BALB/c mouse-embryo cell line BALB/3T3 contain at least two distinct classes of endogenous type-C viral genomes. Spontaneously released endogenous viruses grow well on the mouse cell line NIH/3T3 (N-tropic viruses) but not on the rabbit cell line SIRC. Type-C viruses induced by treatment with BrdU grow well on SIRC (S-tropic viruses) but not in NIH/3T3 or BALB/3T3. BrdU-treated AKR mouse-embryo cells also release an S-tropic virus. N-tropic and S-tropic viruses both have the mouse intraspecies gs-1 and viral RNA-directed DNA polymerase antigenic determinants. DNA.RNA hybridization techniques reveal that the two host-range classes of endogenous viruses are only partially related to each other. Cell transformation facilitates the spontaneous release of the N-tropic viruses; treatment with thymidine analogues induces the production of the S-tropic viruses. Thus, the two classes of viral genomes appear to be subject to different cellular controls.

Animals↗
PubMed1982

T cell subset abnormalities in tissue lesions developing during autoimmune disorders, viral infection, and graft-vs.-host disease.

The authors review a large body of contemporary immunohistologic findings on the tissue distribution of T lymphocytes in normal and pathological conditions. The suggestions for technological advances in this field are: signal amplification using mixtures of monoclonal antibodies directed against different epitopes on the same antigen (e.g. OKT4A+B+D), triple layer amplification systems using hapten-labelled antibodies, and informative double staining methods with combinations of antibodies labelled with different fluorochromes or enzymes. Review of histological observations in a series of human diseases suggests that imbalances of OKT4+ and OKT8+ subsets of T lymphocytes may represent different types of immunoregulatory disorders. Rheumatoid arthritis and sarcoidosis appear to involve a high level of OKT4+ subpopulation response coupled with an associated appearance of a special type of HLA-DR+ macrophages. It remains to be seen whether normal or self-limited immunological responses (early stages of bacterial infection or delayed-type hypersensitivity reactions) produce OKT4+ and macrophage responses that are characteristically different. Meanwhile, excessive levels of OKT8+ cells have been found in a wide range of recognized or presumed immunoregulatory disorders including: graft-vs.-host reaction and viral infections. These disorders, as well as primary biliary cirrhosis and lichen planus, appear to possess both overlapping and disparate clinical characteristics, and the immunohistological observations may reflect the functional heterogeneity of OKT8+ populations in these diseases. These studies show that histologically meaningful heterogeneity can already be demonstrated for the OKT8+ lymphocyte group.

Animals↗
PubMed1993

The current status of viral immunology.

Many aspects of viral immunity, ranging from the molecular and cellular studies of the interaction between viruses and host cells in vitro and the crystalline structures of the MHC and peptides, to the regulation of pathogenesis in experimental animals and humans were discussed at a recent meeting.

Allergy and Immunology↗
PubMedDate not supplied

Spontaneous mutation of RNA tumour viruses.

There are 2 categories of spontaneously occurring avian and mammalian RNA tumour virus mutants: conditional and non-conditional. 1) Conditional mutants are able to replicate in or transform cells only under certain physiological conditions or in certain cells. RNA tumour virus temperature-sensitive mutants, focus-morphology mutants, and host range mutants are spontaneously formed. Some of these conditional mutants probably arise by point mutations in the viral genome. 2) Non-conditional mutants have genetic lesions that render them inactive under all conditions. There are non-conditional spontaneous RNA tumour virus mutants that are missing either the virion envelope glycoprotein or both the envelope glycoprotein and the virion DNA polymerase. These mutants cannot replicate or transform cells. Other spontaneous non-conditional mutants can replicate but are defective in their ability to transform fibroblastoid cells. These spontaneous transformation-defective mutants can have deletions in 10-20% of the genomic RNA. Conditional mutants with an altered host range occur at a high rate of approximately 1 mutation/50 infected cell generations during DNA-to-DNA information transfer. This type of conditional mutation requires cell replication but does not occur frequently either during the original synthesis of viral DNA (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the (RNA-to-DNA information transfer) or during the transcription of progeny viral RNA from the DNA (DNA-to-RNA information transfer). Temperature-sensitive and focus-morphology mutants also have a high rate of spontaneous formation. Non-conditional mutants missing the viral envelope glycoprotein, DNA polymerase, or transformation gene, also appear to be spontaneously formed at a high rate. Normal avian and mammalian cells contain RNA tumour virus-related genes in their DNA. It is hypothesized that these endogenous RNA tumour virus-related genes in normal cells also have a high rate of spontaneous mutation and are involved in neoplastic processes.

Animals↗
PubMed1979

Lymphotropic papovaviruses isolated from African green monkey and human cells.

A lymphotropic papovavirus was isolated from a lymphoblastoid cell line of African green monkey (AGM) cells which also contained a herpesvirus and a paramyxovirus-like agent. The papovavirus was analyzed by restriction endonuclease cleavage; its biochemical and serological crossreactivity with SV40 and host range have been determined. Thus far, only B-lymphoblasts of primate and human origin have been found to be susceptible to infection. Although more than 50% of the tested monkey sera were reactive with antigens of this virus, all human sera tested failed to react. Cleavage patterns and hybridization studies with the viral DNA indicate that the virus represents a novel member of the papovavirus group that is characterized by its lymphotropic host range. Papovavirus particles were also demonstrated in a human lymphoblastoid cell line (CCRF-SB) originally derived from a leukemic child. These cells revealed nuclear fluorescence when tested with human sera, but failed to react with AGM sera. Although characterization of this agent has not yet been completed, available evidence suggests that it represents another lymphotropic papovavirus which seems to be spread within the human population.

Animals↗