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At least 19 recordsLinked to original sources
PubMed1978

Viral immune complexes in systemic lupus erythematosus: C-type viral complex deposition in skin.

Punch biopsies were examined by indirect immunofluorescence for immune complex deposits containing C-type viral antigen. Antisera specific for immunoglobulins and HEL-12 virus mediated fluorescence at the dermal-epidermal junction and in vessel walls of 16 of 16 biopsies involved skin from patients with systemic lupus erythematosus (SLE). Preimmune sera did not mediate fluorescence and gradient purified HEL-12 virus, simian sarcoma virus and baboon endogenous virus but not Rous sarcoma virus blocked the reaction of anti-HEL-12 virus serum with SLE tissue. Ten biopsies from uninvolved skin of the patients with SLE did not react with the antiviral serum, nor did tissue from 9 patients with discoid lupus erythematosus, psoriasis, bullous pemphigoid or normal skin. These data support the hypothesis that C-type viral immune complexes participate in the pathogenesis of SLE.

Animals↗
PubMed1979

Association of simian virus 40 T antigen with simian virus 40 nucleoprotein complexes.

Viral nucleoprotein complexes were extracted from the nuclei of simian virus 40 (SV40)-infected TC7 cells by low-salt treatment in the absence of detergent, followed by sedimentation on neutral sucrose gradients. Two forms of SV40 nucleoprotein complexes, those containing SV40 replicative intermediate DNA and those containing SV40 (I) DNA, were separated from one another and were found to have sedimentation values of 125 and 93S, respectively. [(35)S]methioninelabeled proteins in the nucleoprotein complexes were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In addition to VP1, VP3, and histones, a protein with a molecular weight of 100,000 (100K) is present in the nucleoprotein complexes containing SV40 (I) DNA. The 100K protein was confirmed as SV40 100K T antigen, both by immunoprecipitation with SV40 anti-T serum and by tryptic peptide mapping. The 100K T antigen is predominantly associated with the SV40 (I) DNA-containing complexes. The 17K T antigen, however, is not associated with the SV40 (I) DNA-containing nucleoprotein complexes. The functional significance of the SV40 100K T antigen in the SV40 (I) DNA-containing nucleoprotein complexes was examined by immunoprecipitation of complexes from tsA58-infected TC7 cells. The 100K T antigen is present in nucleoprotein complexes extracted from cells grown at the permissive temperature but is clearly absent from complexes extracted from cells grown at the permissive temperature and shifted up to the nonpermissive temperature for 1 h before extraction, suggesting that the association of the 100K T antigen with the SV40 nucleoprotein complexes is involved in the initiation of SV40 DNA synthesis.

Antigens, Neoplasm↗
PubMed2025

Genomics insight on passion fruit viral disease complexity.

Passion fruit viral diseases pose a significant threat to Kenya's passion fruit industry. To unravel the complexity of these diseases, comprehensive virus surveys were conducted across major passion fruit-growing counties. Passion fruit woodiness disease symptoms, like fruit hardening, chlorotic mottling, and leaf distortion, were prevalent. The study unveiled the first 23 complete genomes of Ugandan passiflora virus (UPV) and two East Asian passiflora distortion virus (EAPDV) in Kenya. UPV showed 99% nucleotide (nt) match to a UPV genome from Uganda and 66% nt identity match to EAPDV. In addition, UPV variants and two partial passion fruit green spot virus sequences and partial (passiflora emaravirus) segment RNA1-5 (novel allexivirus and an emaravirus, respectively) were detected. Phylogenetic analysis revealed distinct lineages (I-III), indicating potential multiple introductions into Kenya. Recombination analysis detected no significant breakpoints. However, the study proposed the renaming of EAPDV to passiflora distortion virus (PDV) and UPV to passiflora virus (PV) for neutral nomenclature, without geographical association. Additionally, the study highlighted the role of coinfections in symptom expression, suggesting a potential synergistic relationship between PV, PDV, and other viruses. The results recommend stringent management strategies and enhanced surveillance to mitigate the economic impact of these viruses on the Kenyan passion fruit industry. The findings from this study underscore the need to strengthen nursery certification programs and pest diagnostic protocols in Kenya. Additionally, enhanced pest surveillance and import regulations are critical to preventing the introduction and spread of emerging plant viral diseases, thereby safeguarding the country's horticultural productivity and biosecurity. To our knowledge, this is the first comprehensive study of viral diseases of passion fruit in Kenya.IMPORTANCEThis study presents the first comprehensive survey of viral pathogens affecting passion fruit in Kenya, identifying Ugandan passiflora virus (UPV) and East Asian passiflora distortion virus (EAPDV) as major contributors. Through genomic sequencing, 23 complete genomes of UPV and two of EAPDV were characterized, revealing a 99% nucleotide (nt) similarity between UPV strains from Uganda and Kenya, and 66% nt match with EAPDV. Phylogenetic analysis identified distinct lineages, suggesting possible multiple viral introductions in Kenya. The study also highlights potential synergistic coinfections between UPV, EAPDV, and other viruses, leading to more severe disease symptoms. In light of these findings, the study proposes renaming EAPDV as passiflora distortion virus and UPV as passiflora virus for a more neutral name classification. The research underscores the urgent need for enhanced surveillance, stringent phytosanitary measures, and improved management strategies to mitigate the threat of viral diseases, to safeguard the Kenyan passion fruit industry, and elsewhere.

Plant Diseases↗
PubMed1979

Histone modifications in simian virus 40 and in nucleoprotein complexes containing supercoiled viral DNA.

Simian virus (SV40) nucleoprotein complexes containing circular supercoiled viral DNA were extracted from infected cells and purified by differential centrifugation. The protein content of these complexes was compared by electrophoresis on 15% acrylamide gels with the protein content of purified SV40 virions and with histones from virus-infected cells. The electrophoretic patterns of histones from each of the sources revealed several major differences. SV40 virions contained histones H3, H2B, H2A, and H4 but not H1. Nucleoprotein complexes and host cells contained all five major histone groups. Relative to cellular histones, virion and nucleoprotein complex histones were enriched 15 to 40% in histones H3 and H4. In addition to the major classes of histones, several subfractions of histones H1, H3, and H4 were observed in acrylamide gels of proteins from SV40 virions and viral nucleoprotein complexes. Acetate labeling experiments indicated that each subfraction of histones H3 and H4 had a different level of acetylation. The histones from SV40 virions and nucleoprotein complexes were acetylated to significantly higher levels than those of infected host cells. No apparent differences in phosphorylation of the major histone groups were observed.

Acetylation↗
PubMed1978

[Circulating immune complexes in acute viral hepatitis, chronic active hepatitis, and periarteritis nodosa (author's transl)].

Circulating immune complexes were determined in patients with acute viral hepatitis, chronic active hepatitis and periarteriitis nodosa with the Raji cell technique. Circulating immune complexes were found in 11/18 HBsAg positive and HBsAg negative cases of acute viral hepatitis. In HBsAg positive chronic active hepatitis immune complexes were detectable in 42/43 cases but only in 1/27 HBsAg negative cases. Ten healthy HBsAg carriers demonstrated no detectable immune complexes. Using FITC conjugated antisera against HBs, HBc, and e antigen, immune complexes could not be found in any case of acute viral hepatitis or chronic active hepatitis. Elution of immune complexes from Raji demonstrated IgG, C'3 and a lack of HBsAg, HBc or e antigen. Immune complexes were present in 4/8 cases with periarteriitis nodosa. Viral components were detectable in one case.

Acute Disease↗
PubMed1976

Fractionation of DNA nucleotide transcripts from Moloney sarcoma virus and isolation of sarcoma virus-specific complementary DNA.

Radioactive DNA complementary to nucleotide sequences in Moloney murine sarcoma virus (MSV) and Moloney leukemia virus (M-MuLV) complex was made by the endogenous reverse transcriptase reaction. These virus stocks contained a threefold excess of MSV over M-MuLV as measured by biological assay. The complementary DNA was an accurate copy of the viral RNA in that 86% of 35S viral RNA hybridized with complementary (cDNA) DNA at a 1.5 to 1 cDNA-RNA molar ratio. The complementary DNA, of a 4-6S size, was fractionated by sequential absorptions with MulV and the feline leukemia virus pseudotype of MSV, [MSV(FeLV)] RNA. In this manner three sets of nucleotide sequences whichrepresent different portions of the MSV viral complex were obtained: a sarcoma virus-specific fraction (cDNAsarc) with sequences that had no homology to M-MuLV RNA but which hybridized to MSV (FeLV) RNA, a sarcoma-leukemia fraction (cDNA common) with sequences common to MSV as well as M-MuLV viral RNA, and a cDNAleuk representing those nucleotide sequences found only in M-MuLV. Hybridization of MSV-MuLV viral 35S RNA with a threefold molar excess of cDNA's revealed that approximately 20% was hybridized with cDNAsarc, whereas approximately 75% was hybridized with cDNAcommon. M-MuLV 35S RNA alone did not hybridize with cDNAsarc but did hybridize 40 and 50% with cDNAleuk and cDNAcommon, respectively. The cDNAsarc represents about 25% of the total MSV sequences, whereas the cDNAcommon represents the remainder of the MSV virus genome. Some cDNAcommon sequences were shared by two other sarcoma viruses and several distinctly different isolates of MulV. In contrast, the MSV "sarc" sequences had little or no homology with two other murine sarcoma virus isolates.

Base Sequence↗
PubMed1977

[Expression of an antigen associated with Gross virus on the surfaces of murine cells producing an oncornavirus from the radioleukemia of C57BL/6 mice].

A leukemogenic viral complex was demonstrated in cultures of 13-3 C cell line derived from a C57BL/6, radiation leukemia virus (RadLV-Rs) induced tumor. Both 13-3C and leukemic cells induced in C57BL/6 mice by 13-3C virus carry a cell surface antigen associated with Gross leukemia virus (GCSAa). These findings point to a close similarity between these antigens and those of murine endogenous ecotropic viruses.

AKR murine leukemia virus↗
PubMed1978

Virus-induced immune complex disease: identification of specific viral antigens and antibodies deposited in complexes during chronic lymphocytic choriomeningitis virus infection.

Structural proteins of LCMV were identified and their role in the immune complex glomerulonephritis of LCMV carrier mice was examined. Purified LCMV contained three major polypeptides, a single nonglycosylated nucleoprotein with an estimated m.w. of 63,000, and two surface glycoproteins of 54,000 and 35,000. Deposition of nucleoprotein antigen in the glomeruli of LCMV carrier mice of several strains was demonstrated by immunofluorescent staining with a monospecific antibody. In addition, Ig eluted from kidneys of three strains of LCMV carrier mice was shown by immune precipitation to react against all of major viral polypeptides of LCMV. Antibody from normal mice, and from mice with immune complex disease unrelated to LCMV did not show deposition of LCMV antigen in glomeruli, and Ig eluted from the kidneys of these mice did not react against LCMV antigens. Hence, mice infected at birth with LCMV and persistently infected throughout their life make antibodies to all the known structural polypeptides of the virus.

Animals↗
PubMed1977

Studies on viral DNA protein complexes isolated at different times after infection of monkey kidney cells with simian virus 40.

The major protein components of the DNA complex, isolated from SV40-infected monkey cells, are the major viral structural polypeptide VP1 and cellular histones. At early times (24 h) after infection, VP1 is present in large amounts relative to histones, whereas at late times (48 h), the complex contains mostly histones. The amount of VP1 in the complex can be correlated to the amount of "free" VP1 present in the cells, i.e. VP1 not yet incorporated into virus particles. At early times about 40% of VP1 is "free" VP1; at late times, most of the VP1 is incorporated into virus particles. In contrast, viral DNA is produced in huge excess and only about 13% is incorporated into virions. In agreement with the above result, we find that only about 16% of the DNA in the DNA complex can be chased into virions. There is, apparently, no turnover of newly synthesized VP1 that is associated with the DNA complex at late times after infection.

Animals↗
PubMed1976

Pathogenesis of cytomegalovirus infection. Distribution of viral products, immune complexes and autoimmunity during latent murine infection.

During studies on the mechanisms of virus latency, reactivation and resultant tissue injury in mice infected with murine cytomegalovirus (MCMV) in utero or at birth, we found the occurrence of three distinct pathological groups. In the first group, mice died within 4 weeks of exposure to virus and showed evidence of tissue injury due to MCMV in multiple tissues and organs of the body. The second group consisted of mice which survived the initial infection and was composed of a minority (about 25%) which shed virus (chronically infected). The third group (about 75%) consisted of mice in which shedding of virus could not be detected (latently infected). Study of the latter group indicated that virus was not detected in brain, thymus, liver, kidneys, urine or serum by co-cultivation techniques or by cellular DNA-MCMV DNA hybridization. In contrast, virus could be activated from spleen cells by co-cultivation with allogenic but not syngeneic feeder cells and MCMV-DNA was detected in amounts equivalent to 3 to 4 virus genomes per 100 spleen cells. In both the latently infected and chronically infected mice, in all strains studied evidence of virus-antivirus immune complex deposits in the renal glomeruli occurred. Only one of the six infected strains (C57 Br/cdJ) studied showed manifestations of autoimmune disease with the formation of antibodies to nuclear antigens, DNA and soluble nucleoprotein.

Animals↗
PubMed1975

Synthesis of fibroma viral deoxyribonucleic acid complexes in rabbit kidney cells.

Cytoplasmic extracts of primary rabbit kidney cells inoculated with fibroma virus revealed 2 peaks of DNA complexes (120S and greater than or equal to 410S) in a linear sucrose gradient. Pulse-chase experiments demonstrated a shift in the gradient profile of lighter complexes toward heavier complexes. Synthesis of DNA complexes was inhibited by adding puromycin or actinomycin D. The DNA from virus-infected cultures hybridized 7 to 9 times greater with fibroma virus DNA than did the DNA from noninfected cultuures. The DNA complexes became increasingly resistant to deoxyribonuclease digestion as a function of time during viral growth cycle and produced tumors in rabbits.

DNA, Viral↗