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PubMed2026

Mycodnaviridae is a clade of giant viruses that persistently infect zoosporic fungi.

Giant viruses of the phylum Nucleocytoviricota have emerged as particularly notable due to their increasingly recognized impacts on eukaryotic genome evolution. Their origins are hypothesized to predate or coincide with the diversification of eukaryotes, and they have been detected in hosts that span the eukaryotic tree of life. But surprisingly, such viruses have not been definitively found in Kingdom Fungi, though earlier genomic and metagenomic work suggests putative associations. Here we report both "viral fossils" and active infection by giant viruses in fungi, particularly in the zoosporic phyla Blastocladiomycota and Chytridiomycota. The recovered viral assemblies span up to 350 kb, encode over 300 genes, and form a monophyletic family-level clade within the Nucleocytoviricota related to orders Imitervirales and Algavirales, which we name Mycodnaviridae. We observed variation in infection status among the isolates including apparent active infection and transcriptionally suppressed states, suggesting that viral activation may be constrained to certain life stages of the host. Our experimental findings add to the limited natural virus-host systems available in culture for the study of giant viruses and expand the known host range of Nucleocytoviricota into a new kingdom that contains many model species. Mycodnaviridae have a global distribution, which invites inquiry into the implications of these infections for host traits, host genome evolution, and the metabolic impacts on ecosystems.

Giant Viruses↗
PubMedDate not supplied

Persistent infections in chronic Chagas' disease patients treated with anti-Trypanosoma cruzi nitroderivatives.

We used a molecular method and demonstrated that treatment of the chronic human Trypanosoma cruzi infections with nitroderivatives did not lead to parasitological cure. Seventeen treated and 17 untreated chronic Chagas' disease patients, with at least two out of three positive serologic assays for the infection, and 17 control subjects formed the study groups. PCR assays with nested sets of T. cruzi DNA primers monitored the efficacy of treatment. The amplification products were hybridized to their complementary internal sequences. Untreated and treated Chagas' disease patients yielded PCR amplification products with T. cruzi nuclear DNA primers. Competitive PCR was conducted to determine the quantity of parasites in the blood and revealed < 1 to 75 T. cruzi/ml in untreated (means 25.83+/-26.32) and < 1 to 36 T. cruzi/ml in treated (means 6.45+/-9.28) Chagas' disease patients. The difference between the means was not statistically significant. These findings reveal a need for precise definition of the role of treatment of chronic Chagas' disease patients with nitrofuran and nitroimidazole compounds.

Animals↗
PubMed1989

State of hepatitis B virus DNA in peripheral blood mononuclear cells from persistently infected individuals: correlation with e antigen and viral DNA in the serum as well as with the activity of liver disease.

Peripheral blood mononuclear cells (PBMC) were harvested from 76 asymptomatic carriers of hepatitis B virus (HBV) and 100 patients with type B chronic liver disease. DNA was extracted from cells and tested for the binding with radiolabeled HBV DNA probe by Southern blot hybridization technique. Among 34 asymptomatic carriers who had hepatitis B e antigen (HBeAg) and HBV DNA in the serum, HBV DNA was detected in 29 (85%) PBMC. In remarkable contrast, of the remaining 42 carriers seronegative for HBeAg, only 1 (2%) had HBV DNA in the serum, and none exhibited HBV DNA in PBMC. Among 32 patients seropositive for HBeAg, HBV DNA was detected in 28 (88%) sera, and in 24 (75%) PBMC. Of 68 patients seronegative for HBeAg, HBV DNA was found in 10 (15%) sera, and in 7 (10%) PBMC. Among 62 cases with HBV DNA in PBMC, only 1 had it integrated into the host's DNA. The remaining 61 had free HBV DNA in PBMC. Only 8 of them possessed replicative intermediate forms of HBV DNA, with molecular sizes less than 2.0 kilobases as observed in liver infected with HBV, and they all were patients with chronic active hepatitis. HBV DNA was not detectable in PBMC from 172 controls comprising 44 healthy individuals and 128 patients with non-A, non-B hepatitis. Based on these results, the state of HBV DNA in PBMC reflects the phase of HBV infection with HBeAg in the serum, and a high activity of hepatitis accompanied by active HBV replication.

Animals↗
PubMed1984

Genetic resistance of mice to persistent infection with Mycobacterium lepraemurium in vitro: association with macrophage bactericidal responsiveness to lymphokines and dissociation from production of hydrogen peroxide by macrophages.

Peritoneal and splenic adherent macrophages (SAC) from M. lepraemurium susceptible (C3H/HeJ) and resistant (C57B1/6J) mice were studied for their abilities to generate H2O2 in vitro. Unexpectedly, SAC from the susceptible C3H/HeJ strain produced more H2O2 than those of the resistant C57BL/6J. In vivo sensitization with M. bovis (BCG), or C. parvum increased production of H2O2 by SAC from both strains, whereas in vivo sensitization with M. lepraemurium enhanced H2O2 production only in the C3H/HeJ susceptible strains. In vitro addition of a crude lymphokine enhanced H2O2 production by C3H/HeJ SAC more than by C57BL/6J SAC. In vitro addition of M. lepraemurium caused an inhibition of H2O2 production by SAC from both strains but the inhibition was greater for the resistant C57BL/6J strain. M. lepraemurium phagocytosed in vitro by untreated peritoneal macrophages of both mouse strains were morphologically altered to the same extent. However, the addition of lymphokine dramatically increased the degree of bacterial lysis in only the C57BL/6J strain. These results, support the view that H2O2 plays a limited, if any, role in the protection of the host from M. lepraemurium and may even contribute to susceptibility by inhibiting the host's immune response.

Animals↗
PubMed1976

Persistent infection of cells in culture by respiratory syncytial virus.

The virus-cell relationship of RS virus and the HEp-2 cell line has been examined. The production of cytopathic effect (c.p.e.) on HEp-2 cells has been found to be dependent upon the passage level of the cell line. Cells at lower passage levels exhibit c.p.e. in the form of syncytium formation, while those at higher passage levels no longer exhibit this effect. Cells infected at higher passage levels are covertly infected and continue to produce large amounts of infectious virus which remains cell-associated. On continued passage, these cells remain infected with virus but show no c.p.e. and release little if any infectious virus into the medium. Examination of the RNA species present in infected cells revealed that similar species are present in both the overtly and covertly infected cells.

Cell Line↗