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PubMed1975

Hepatitis A. Perspectives and recent advances.

The basis for the epidemiologic and etiologic differentiation of two major forms of viral hepatitis, hepatitis A and B, was established in a series of studies undertaken between 1930 and 1970. Final recovery and visualization of the presumed etiologic agent of hepatitis A was not, however, accomplished until the technique of immune electron microscopy was applied to the examination of specimen materials collected from individuals in the early acute stages of infection. Morphologically homogeneous virus-like particles of 27 nm diameter have now been recovered from stools of patients with hepatitis A ill from a variety of sources. Antibody to these particles has been shown to develop during the course of infection with hepatitis A but not with hepatitis B and disease has been induced in nonhuman primates inoculated with purified particle containing fractions. The classification of hepatitis A virus has not been conclusively established, but it would appear to be either a parvovirus or an enterovirus.

Antibodies, Viral↗
PubMed2001

A clinicopathological study of acute hepatitis in heavy drinkers, unrelated to hepatitis A, B, or C viruses.

BACKGROUND: There are six histological classifications of alcoholic liver disease (ALD) in Japan. However, it is unclear whether all cases of the disease conform to these criteria. This study investigated the clinicopathological features of eight histologically unusual cases of ALD. METHODS: The characteristic features of alcohol drinking behavior, subjective and objective symptoms, laboratory data on admission, and progress after admission were analyzed for eight patients with acute-onset hepatitis. RESULT: The eight patients showed histologically acute hepatitis, with much spotty necrosis that contained granular ceroid pigment by Kupffer cells, which indicated acute parenchymal damage of the liver, but with no Mallory bodies and unremarkable intrasinusoidal neutrophilic infiltration. The only etiological factor for all the cases was habitual alcohol consumption, with increased consumption just before the onset of symptoms. In five cases that were tested, the patients were negative for hepatic viral markers, which included hepatitis G virus RNA and TT virus DNA. CONCLUSION: Some cases of ALD may not conform to the current histological classifications in either Japan or Western countries. It seems natural to consider that these cases are developed by other, unknown causes that overlap with ALD rather than as a result of damage from alcoholic overload.

Acute Disease↗
PubMed1991

Structural comparison of the external glycoproteins of human and simian immunodeficiency virus.

The structural variability of the external glycoproteins of primate immunodeficiency viruses, has, so far, been investigated exclusively by sequence comparison of the respective proviral genomes. We have examined the structural relationship amount the external glycoproteins from three specific human immunodeficiency viruses (HIF-1, HIV-2), three specific simian immunodeficiency viruses from macaques (SIVmac) and three specific SIV from African green monkeys (SIVagm) by peptide mapping. Differences among glycoproteins were most pronounced between HIV-1 and SIVmac, as well as HIV-2. Two specific glycoproteins from independent SIVagm isolates were closely related to HIV-1, whereas the glycoprotein from a third SIVagm isolate was more similar to those of SIVmac and HIV-2. Our analysis reflects the classification of primate immunodeficiency viruses into three groups, the HIV-2 and SIVmac viruses, the green monkey isolates and HIV-1.

Amino Acid Sequence↗
PubMed2004

Lessons from the study of T-cell differentiation in persistent human virus infection.

Confusion surrounds the current classification of memory and effector T-cell subsets and there is a lack of consistency in the use of these terms between human and murine studies. The development of peptide-HLA tetrameric complexes ("tetramers") that accurately identify virus-specific T cells and can be used with a range of cell surface and intra-cellular markers has provided further insights in our understanding of the process of T-cell differentiation, or post-thymic development. We propose that T-cell differentiation subsets in human viral infection should be regarded as distinct from the current definitions of memory and effector cells; further work is needed to reveal the role of the differentiation process in anti-viral immunity.

Cell Differentiation↗
PubMed2006

Rapid diagnosis of avian influenza (AI) and assessment of pathogenicity of avian H5 and H7 subtypes by molecular methods.

Avian influenza (AI) is a highly contagious viral disease of poultry that is found worldwide. There are two forms of AI: a mild form called low pathogenicity avian influenza (LPAI), and a severe form called highly pathogenic avian influenza (HPAI). HPAI is associated with the H5 and H7 subtypes of AI virus (AIV) and is subject to Federal control and International reporting. A real-time reverse transcription-polymerase chain reaction (rRT-PCR) assay has been developed and validated that can help in the early detection of AI outbreaks. The rRT-PCR assay can also be used to identify infections caused by H5 and H7 subtypes of AIV New isolates of AIV must be characterized as LPAI or HPAI for reporting and control purposes. The criteria for classification of an AI virus as HPAI are defined by the World Organization for Animal Health (OIE); the definition includes a virulence and a molecular criterion. The virulence requirement for HPAI is defined as an AIV killing 75% or more of eight inoculated chickens within 10 days. The molecular criterion is the presence of multiple dibasic amino acids at the proteolytic cleavage site of the haemagglutinin (H) protein. All HPAI viruses isolated before 2002 fulfilled both the virulence and molecular criteria. Consequently, nucleotide sequencing of the H gene and deduction of the amino acid motif at the H cleavage site has been successfully used to assess the virulence of H5 and H7 AIVs rapidly. Since 2002, however, there have been three outbreaks of HPAI where the viruses responsible for the outbreaks have either fulfilled the virulence criterion or the molecular criterion, but not both.

Amino Acid Sequence↗
PubMed1981

Virion polypeptide heterogeneity among virulent and avirulent strains of eastern equine encephalitis (EEE) virus.

Comparative analysis of structural virion polypeptides of 24 selected EEE virus strains, representing North and South American types, was performed by one-dimensional discontinuous sodium dodecyl sulfate (SDS)-polyacrylamide-gel electrophoresis (PAGE). The structural proteins of different EEE virus isolates, resolved by this method, exhibited mol.wts. values in the range of 57-60 X 10(3) for (E-1), 51-54 X 10(3) for (E-2) and 35-38 X 10(3) daltons for the core (NP) nucleocapsid. The exception was the South American human lethal virus, TRVL-89287 strain, which was shown to possess only a single envelope glycoprotein. The high molecular weight envelope (E-1) glycoprotein species was absent or co-migrated adjacent to the smaller envelope (E-2) glycoprotein. Results indicated similarities in the core (NP) proteins, however greater variability in the envelope (E-/ and/or E-2) glycoproteins. Based on these variations seven distinct profiles could be observed among the EEE virus strain studied. The classification based on the patterns of structural polypeptides obtained by SDS-PAGE of these strains does not correlate well with any other previously reported in vitro characteristics (antigenic subtypes, HTP elution profiles) nor with the in vivo virulence markers.

Alphavirus↗
PubMed2006

Cytotoxic T-lymphocyte antigen 4 gene polymorphisms and susceptibility to chronic hepatitis B.

AIM: To assess the three polymorphism regions within cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene, a C/T base exchange in the promoter region -318 (CTLA-4 -318C/T), an A/G substitution in the exon 1 position 49 (CTLA-4 49A/G), a T/C substitution in 1172 (CTLA-4 -1172T/C) in patients with chronic hepatitis B. METHODS: Fifty-one patients with chronic hepatitis B virus infection and 150 healthy subjects were recruited sequentially as they presented to the hepatic clinic. Classification of chronic hepatitis B virus (HBV)-infected patients was as asymptomatic carrier state (26 patients) and chronic hepatitis B (25 patients). Genomic DNA was isolated from anti-coagulated peripheral blood Buffy coat using Milleros salting-out method. The presence of the CTLA-4 gene polymorphisms was determined using polymerase chain reaction amplification refractory mutation system (ARMS). RESULTS: We observed a significant association between -318 genotypes frequency (T+C-, T+C+, T-C+) and susceptibility to chronic hepatitis B (P=0.012, OR=0.49, 95%CI: 0.206-1.162). However, we did not observe a significant association for +49 genotype frequency (T+C+, T+C- T-C+) and -1172 genotype frequency (C+T+, T+C- C+T-) and state of disease. CONCLUSION: Our results suggest that CTLA-4 gene polymorphisms may partially be involved in the susceptibility to chronic hepatitis B.

Adult↗
PubMed1993

Classification and diagnostic criteria for oral lesions in HIV infection. EC-Clearinghouse on Oral Problems Related to HIV Infection and WHO Collaborating Centre on Oral Manifestations of the Immunodeficiency Virus.

A consensus has been reached on the classification of the oral manifestations of HIV infection and their diagnostic criteria, based on presumptive and definitive criteria. The former relate to the initial clinical appearance of the lesion and the latter are often the result of special investigations. Candidiasis, hairy leukoplakia, specific forms of periodontal disease [linear gingival erythema, necrotising-(ulcerative) gingivitis and necrotising(ulcerative) periodontitis], Kaposi's sarcoma and non-Hodgkin's lymphoma are strongly associated with HIV infection. Lesions less commonly associated with HIV infection and lesions seen in HIV infection, but not indicative of the disease, are also listed.

Candidiasis, Oral↗
PubMed2005

Extrahepatic manifestations in patients with chronic hepatitis C virus infection.

PURPOSE OF REVIEW: Chronic hepatitis C virus infection often has autoimmune clinical and analytic features. This review analyzes recent data on the close association of chronic hepatitis C virus infection with autoimmune and lymphoproliferative processes. RECENT FINDINGS: Hepatitis C virus infection has been associated with both organ-specific (thyroiditis, diabetes) and systemic autoimmune diseases. Experimental, virologic, and clinical evidence has demonstrated a close association between hepatitis C virus infection and Sjögren syndrome, with hepatitis C virus-associated Sjögren syndrome being indistinguishable in most cases from the primary form. With respect to rheumatoid arthritis, patients with hepatitis C virus-related polyarthritis and positive rheumatoid factor may fulfill the classification criteria for rheumatoid arthritis. Hepatitis C virus has also been associated with an atypical presentation of antiphospholipid syndrome, as well as with the development of sarcoidosis. A higher prevalence of hematologic processes in patients with hepatitis C virus infection has recently been reported, including cytopenias and lymphoproliferative disorders. Recent data are available on the use of new immunosuppressive and biologic agents (mainly mycophenolate mofetil, anti-tumor necrosis factor agents, and rituximab) in patients with hepatitis C virus infection and autoimmune or lymphoproliferative manifestations. SUMMARY: There is increasing evidence of a close association of hepatitis C virus infection with autoimmune and hematologic processes. The sialotropism of hepatitis C virus may explain the close association with Sjögren syndrome, and its lymphotropism links the virus to cryoglobulinemia, autoimmune cytopenias, and lymphoma. The substantial overlap between cryoglobulinemic features and the classification criteria for some systemic autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa) make the differentiation between mimicking and coexistence difficult.

Autoimmune Diseases↗
PubMed1975

Comparison of the sensitivity to ultraviolet irradiation of reovirus 3 and some viruses of the Kemerovo group.

The kinetics of UV inactivation of the tick-borne Kemerovo (strain R-10) and Lipovnik (strain Lip-91) viruses which have been preliminarily classified as possible members of the Reovirus group was examined. Reovirus 3 and Sindbis virus served as reference double-stranded RNA and single-stranded RNA viruses, respectively. The parameters of UV inresembled those of Reovirus 3. This is consistent with their tentative classification as reovirus-like viruses.

Animals↗
PubMed1980

OK10, an avian acute leukemia virus of the MC 29 subgroup with a unique genetic structure.

The RNA of defective avian acute leukemia virus OK10 was isolated from a defective virus particle, released by OK10-transformed nonproducer avian fibroblasts, as a 60S complex consisting of 8.6-kilobase subunits. Oligonucleotide fingerprinting and RNA.cDNA hybridization identified two sets of sequences in OK10 RNA: group-specific sequences, which are related to all nondefective members of the avian tumor virus group, and a sequence closely related to the subgroup-specific sequences (mcv) of the myelocytomatosis virus (MC29) subgroup of avian acute leukemia viruses. Hence, OK10 is classified as a member of the MC29 subgroup of avian tumor viruses, in agreement with classification based on its oncogenic spectrum. The group-specific sequences of OK10 RNA include partial (Delta) pol and env genes, a c-region, and, unlike those of all other members of the MC29 subgroup, a complete gag gene. Oligonucleotide mapping revealed 5'-gag-Deltapol-mcv-Deltaenv-c-3' as the order of the subgroup-specific and group-specific elements of OK10 RNA. The genetic unit gag-Deltapol-mcv, measuring approximately 6.4 kilobases, codes for the nonstructural, presumably transforming, 200,000-dalton OK10-specific protein and also includes the gag gene coding for the internal virion proteins. Because gag is the only intact virion gene shared in addition to regulatory RNA sequences between OK10 and nondefective avian tumor viruses, it is concluded that the gag gene is sufficient for the formation of a defective virus particle. Comparisons among the RNAs and gene products of different viruses of the MC29 subgroup show that they share 5'-terminal gag-related and internal mcv sequences but differ from each other in intervening gag-, pol-, and mcv-related sequences. It follows that the probable transforming genes and their protein products have two essential domains, one consisting of conserved 5' gag-related and the other of 3' mcv-related sequence elements. In the light of this and previous knowledge we can now distinguish two designs among five different transforming onc genes of avian tumor viruses: onc genes with coding sequences unrelated to virion genes, like those of Rous sarcoma virus and avian myeloblastosis virus, and onc genes with coding sequences that are hybrids of virion genes and specific sequences, like those of the MC29 subgroup viruses, of avian erythroblastosis virus, and of Fujinami sarcoma virus.

Animals↗
PubMed2000

Detection of diverse variants of human immunodeficiency virus-1 groups M, N, and O and simian immunodeficiency viruses from chimpanzees by using generic pol and env primer pairs.

Human immunodeficiency virus type 1 (HIV-1) infection of humans is the result of independent cross-species transmissions of simian immunodeficiency viruses (SIVcpz) from naturally infected chimpanzees (Pan troglodytes troglodytes) to man. To develop a polymerase chain reaction-based assay capable of detecting members of all major phylogenetic SIVcpz and HIV-1 lineages (groups M, N, and O), primer pairs in conserved pol and env regions were designed. Both primer sets amplified </=10 copies of selected group M reference clones (subtypes A-H), proviral DNA or RNA of group N (YBF30), and group O of HIV-1 and also amplified divergent SIVcpz from cultured isolates (SIVcpzGAB1 and SIVcpzANT), uncultured spleen tissue (SIVcpzUS), and plasma (SIVcpzANT and SIVcpzUS). Sequences of the 2 amplicons (445 bp for gp41 and 261 bp for integrase) are of sufficient length for phylogenetic analyses, allowing both group and subtype classifications of the human viruses. Finally, both primer pairs are highly sensitive (>99%) in amplifying viral sequences from plasma taken from patients infected with HIV-1 group M (n=226) and O (n=17) viruses.

Animals↗
PubMed1988

[Classification of manifestations in the course of infection with the human immunodeficiency virus (HIV)].

The vast number of symptoms, diseases and findings, which can be observed in the course of HIV-infection, required an arrangement in a systematic order. The classification system for adults of the Centers for Disease Control (CDC) distinguishes between 4 groups and some subgroups. Group I includes acute infection, group II asymptomatic infection, group II persistent generalized lymphadenopathy, group IV other diseases. Subgroup IV.A. stands for constitutional disease, IV.B. neurologic disease, IV.C. secondary infectious diseases, IV.D. secondary cancers and IV.E. other conditions. A somewhat different classification system is needed for children under 13 years of age. Class P-0 comprises indeterminate infection, P-1 asymptomatic infection and P-2 symptomatic infection. Subclass P-1.-A. concerns normal immune function, P-1.B. abnormal immune function, P-1.C. immune function not tested, P-2.A. nonspecific findings, P-2.B. progressive neurologic disease, P-2.C. lymphoid interstitial pneumonitis, P-2.D. secondary infectious diseases, P-2.E. secondary cancers and P-2.F. other diseases possibly due to HIV-infection.

Acquired Immunodeficiency Syndrome↗
PubMed2026

Deep learning-assisted, pathogenesis-informed lung histopathology scoring in preclinical mouse models of SARS-CoV-2 and influenza A infection.

INTRODUCTION: SARS-CoV-2 and influenza A virus (IAV) cause viral pneumonia, yet their lung lesions evolve with distinct spatial organization and resolution-phase architecture. In preclinical murine studies, H&E histopathology is a primary endpoint, but burden-focused semiquantitative scoring can miss pathogen- and phase-specific differences in lesion topology, compartmental involvement, inflammatory organization, and repair. We aimed to define virus- and phase-specific morphologic signatures and translate them into a practical, pathogenesis-informed scoring guide, supported by whole-slide convolutional neural network (CNN) analysis with class activation mapping (CAM). METHODS: Mice were infected under standardized conditions and evaluated during the early, peak-injury, and late phases of infection, corresponding to 2~3, 5~8, and 14 days post-infection (dpi), respectively. Lungs were assessed by H&E with semiquantitative scoring and by immunostaining to map viral antigen distribution and epithelial tropism. Whole-slide CNN models were trained for virus- and phase-specific classification, and CAM localized discriminative regions. RESULTS: Dose titration established reproducible lethal and sublethal infection conditions for both viruses. Viral antigen kinetics diverged, with SARS-CoV-2 peaking early and declining toward clearance by the resolution phase, whereas IAV peaked later and declined by the resolution phase, paralleling distinct injury-repair trajectories. CNN/CAM analysis distinguished virus- and phase-specific histologic patterns across the early, peak-injury, and resolution phases of infection and highlighted spatial signatures consistent with expert review. At the peak-injury phase, SARS-CoV-2 lungs showed broad alveolar/interstitial involvement, whereas IAV exhibited bronchocentric inflammatory organization. During the resolution phase, IAV showed prominent epithelial regeneration with remodeling-forward architecture, while SARS-CoV-2 more often retained localized residual inflammatory foci. Across both infections, tissue inflammatory composition shifted over time, with higher neutrophil representation during the peak-injury phase and a relative increase in lymphocytic representation during the resolution phase. Integrating lesion topology/distribution, edema, epithelial injury-regeneration, remodeling features, and lymphocyte predominance, we proposed a pathogen-resolved, phase-informed histopathology scoring guide with recommended evaluation windows for each model. CONCLUSION: Together, these findings define virus- and phase-specific morphologic programs that inform respiratory virus pathogenesis in mice and can be translated into practical scoring criteria for preclinical respiratory virus studies.

Animals↗
PubMed1992

Potyviruses, chaos or order?

At first potyviruses were easily distinguished by biological and serological properties because only a few were known and information on their host ranges was limited. The first evidence of serological cross reaction between two of these viruses was reported in 1951 and was further corroborated for three obviously distinct members of the group in 1960. In 1968 attention was drawn to the fact that some legume and non-legume potyviruses have much wider host ranges than previously known and that within the potyvirus group there is as much biological variation within viruses and overlap between viruses as there is in serology. The concept of continuity within the group was soon supported by others and became known as the "continuum hypothesis." Results with highly sensitive serological methods using polyclonal antisera were conflicting, and nucleic acid hybridization techniques did not unambiguously discriminate between potyviruses. Recent results, obtained with antibodies directed toward epitopes located in the N-termini of the coat proteins of potyviruses, suggest that there are ways to more definitely group strains of one potyvirus and distinguish them from other potyviruses. However, there are exceptions to this rule, as in the case of bean yellow mosaic virus and clover yellow vein virus which are clearly distinct in host range, inclusion bodies, and migration velocity of coat protein, but which still react with antibodies to the N-terminal epitopes of one virus. So the question remains of whether coat-protein properties, especially the serological reactivity of N-termini, which do not alter overall virus integrity when lost, sufficiently represent the genome of a pathogenic virus entity as a single criterion for classification.

Capsid↗
PubMed1990

Watermelon mosaic virus II and zucchini yellow mosaic virus: cloning of 3'-terminal regions, nucleotide sequences, and phylogenetic comparisons.

The 3'-terminal genomic regions of an isolate of watermelon mosaic virus II (WMVII) and a Florida isolate of zucchini yellow mosaic virus (ZYMV-F) have been cloned. The nucleotide sequence of the WMVII cDNA clone shows the presence of the large nuclear inclusion protein gene, the coat protein gene and 3' untranslated region. The nucleotide sequence of a ZYMV-F cDNA clone shows the presence of the coat protein gene and 3' untranslated region. Comparisons of the nucleotide and deduced amino acid sequences of these clones with those from other potyviruses show that WMVII and the soybean mosaic virus N strain are closely related, thus supporting their classification as different strains of the same virus. Our comparisons also indicate that ZYMV-F is a distinct potyvirus type and that its closest relative is WMVII. Phylogenetic analysis using the most-parsimonious branching arrangement derived from the alignment of coat protein gene sequences suggests the existence of two major potyvirus groupings.

Amino Acid Sequence↗