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At least 19 recordsLinked to original sources
PubMed2026

Hemotropic mono- and coinfections in Colombian ruminants: descriptive occurrence and host-related factors associated with coinfection in cattle.

Hemotropic pathogens such as Anaplasma, Babesia, Mycoplasma, and Trypanosoma are endemic to cattle and can cause coinfections, complicating disease dynamics and control. However, the host-related factors influencing these infections under tropical conditions remain poorly understood. This study aimed to investigate the occurrence of hemotropic monoinfections and coinfections in ruminants tested for hemotropic pathogens and to identify host-related factors associated with coinfection in cattle under field conditions in Colombia. A total of 104 animals were included: 91 cattle, 10 buffaloes, and 3 goats. Among the cattle, 34 (37.4%) exhibited monoinfections, 47 (51.6%) had coinfections, and 10 tested negative. In buffaloes, seven (70%) presented monoinfections, and two (20%) presented coinfections; in goats, one had a monoinfection, and one had a coinfection, most frequently involving Mycoplasma spp. The predominant coinfection patterns were Anaplasma&#x2009;+&#x2009;Mycoplasma and Mycoplasma&#x2009;+&#x2009;Trypanosoma, particularly in Bos indicus cattle. Bivariate and multivariable analyses revealed that breed was the strongest predictor of coinfection, with animals of less common breeds showing 93% lower odds (aOR&#x2009;=&#x2009;0.07; 95% CI: 0.02-0.30; p&#x2009;<&#x2009;0.001). Bos taurus individuals also tended toward lower odds of coinfection in the multivariable model, although this trend did not reach statistical significance. Our findings demonstrate a high frequency of hemotropic coinfections in cattle, particularly those involving Mycoplasma spp., and highlight the influence of host-related factors on infection dynamics. These results underscore the importance of integrating demographic and genetic information into surveillance and prevention strategies to improve the management of hemotropic infections in tropical livestock systems.

Animals↗
PubMed1992

Strain-specific selection of genome segments in avian reovirus coinfections.

To determine whether selection of genome segments in coinfections is strain-specific, chicken embryo fibroblasts were coinfected with avian reovirus strain 883 and one of three other avian reovirus strains (176, S1133 and 81-5). Viral progeny from each coinfection (883 x 176, 883 x S1133 or 883 x 81-5) was serially passaged at a low m.o.i. The electropherotypes of the coinfection progeny and those of the plaque-derived clones obtained from passages 1 and 20 were analysed. Two 883 segments (M2 and S2) were found to be selected in the 883 x 176 coinfection, three 883 segments (M2, M3 and S2) in the 883 x S1133 coinfection, and only one 883 segment (M3) in the 883 x 81-5 coinfection, i.e. different 883 genome segments were selected in the three coinfections. It was, therefore, concluded that selection of genome segments in a coinfection of a given cell line is virus strain-specific. The selection of genome segments in coinfections was shown to be due to enhanced infectivity of the reassortants that were formed in the coinfections. In addition, defective interfering particles that lack the S1 segment were identified in the 883 x 81-5 coinfection progeny following serial passage. Selection of genome segment(s) in coinfections as described herein may have potential importance on the effect and production of divalent or multivalent vaccines.

Animals↗
PubMed1991

Altered HIV expression and EBV-induced transformation in coinfected PBLs and PBL subpopulations.

Human immunodeficiency virus (HIV) IIIB expression and Epstein-Barr virus (EBV) B95.8-induced transformation were studied during coinfection. Coinfection of peripheral blood lymphocyte (PBL) cultures with HIV and EBV resulted in down-regulation of HIV expression. EBV-induced and spontaneous transformation were markedly reduced in PBL cultures exposed to HIV before EBV. On the other hand, transformation was enhanced when PBL cultures were infected with HIV either simultaneous to or after EBV. Reconstitution of EBV-infected B cell cultures with autochthonous T cells demonstrated that HIV-infected T cells had a reduced ability to inhibit EBV-induced transformation. PHA stimulation of HIV-infected T cells eliminated their ability to inhibit EBV-induced transformation. Lymphoblastoid cell lines (LCLs) established from coinfected PBLs expressed B cell markers and were EBV positive, while a large proportion of the LCLs expressed HIV antigens, released reverse transcriptase activity into the supernatant, and produced syncytia when cocultivated with indicator cell line SupT1. HIV provirus could be detected in LCLs established from coinfected cultures by PCR amplification using specific sets of amplimers for gag and env genes of HIV. To more closely examine the role of various cell types in lymphocyte transformation and HIV replication during coinfection, experiments were carried out using subpopulations enriched for either B or T cells. Simultaneous coinfection of purified B cells with EBV and HIV resulted in a marked reduction of HIV expression, whereas EBV-induced transformation was enhanced. In contrast, spontaneous B cell transformation was inhibited by HIV. A proportion of LCLs established from purified B cells coinfected with EBV and HIV expressed HIV antigens, released reverse transcriptase activity, and produced syncytia on SupT1 cells. These results demonstrate that the IIIB strain of HIV and B95.8 strain of EBV can interact during coinfection of B cells to alter the course of virus expression.

B-Lymphocytes↗
PubMed1991

Direct binding of complement component C1q to human immunodeficiency virus (HIV) and human T lymphotrophic virus-I (HTLV-I) coinfected cells.

Previous studies have shown that coinfection of the human T lymphotrophic virus type I (HTLV-I) chronically infected cell line MT4 with human immunodeficiency virus type 1 (HIV-1) results in cells which spontaneously activate complement via the classical pathway. This complement activation was antibody independent, yet required C2, suggesting either direct C1, C4, or C2 activation. Because some animal retroviruses have been shown to bind human C1q directly, the present study investigated the possible direct binding of C1q by HIV coinfected MT4 cells. Coinfected cells bound both C1q present in serum and highly purified C1q. Binding of C1q resulted in formation of active C1 on the cell surface, which could in turn activate complement as shown by C4 consumption. The C1q binding was not HIV-isolate specific since infection of MT4 cells with any of three diverse isolates all induced C1q binding. Purified collagen-like region (CLR) and globular region (GR) fragments of C1q both bound to coinfected cells, suggesting a mechanism of binding by C1q similar to that of fibronectin-C1q binding. However, culture of coinfected cells in serum-free (fibronectin-free) medium did not reduce C1q binding. A second HTLV-I chronically infected line, SLB-1, also displayed increased binding of C1q after HIV infection. The H9 cell line, which is not HTLV-I infected, did not bind C1q after HIV infection. These results suggest that a retrovirus protein expressed by coinfected cells directly binds C1q resulting in classical complement activation. This type of activation may have profound biological effects in persons coinfected with HIV-1 and HTLV-I.

Cell Line↗
PubMed2026

Influenza A Virus Coinfection Alters Streptococcus pneumoniae Gene Expression during Upper Respiratory Tract Colonization.

Streptococcus pneumoniae (Spn) asymptomatically colonizes the upper respiratory tract (URT), a niche from which it can transmit to another host or cause invasive disease in the same host. The in vivo transcriptional adaptations that Spn undergoes during nasopharyngeal colonization, particularly during influenza A virus (IAV) coinfection, are poorly understood. Here, we leveraged an established infant mouse model of colonization, shedding, and transmission to perform genome-wide transcriptomic profiling of Spn during mono- and during IAV co-infection. Compared with broth-grown controls, pneumococci isolated from the URT exhibited distinct transcriptional programs, with over 200 genes differentially expressed across time points. Genes involved in carbohydrate uptake and metabolism, glycan degradation, amino sugar and nucleotide sugar metabolism, and amino acid biosynthesis were consistently enriched during colonization, highlighting metabolic adaptation to the nasopharyngeal niche. In contrast, IAV coinfection induced a markedly distinct transcriptional signature, including upregulation of branched-chain amino acid biosynthesis, bacteriocin production, and phosphate acquisition systems. Notably, the pilus islet-1 locus was upregulated during Spn-IAV coinfection. Functional studies demonstrated that while the pilus was dispensable for colonization under mono- and coinfection conditions, it promoted high-shedding events and enhanced inflammatory responses during IAV coinfection. However, reduced inflammation and reduced high shedding events from pups inoculated with a pilus-deficient mutant did not alter transmission frequency in the infant mouse model. Collectively, our findings define the in vivo transcriptional landscape of Spn during URT colonization and reveal distinct bacterial adaptations during viral coinfection, providing insight into mechanisms that influence pneumococcal persistence, inflammation, and transmission.

Journal Article↗
PubMedDate not supplied

[HTLV1 and coinfections].

After reminding the epidemiology of the HTLV1 infection the authors sum up the actually recommended diagnosis procedure. --Case finding by ELISA, confirmation by WESTERN-BLOT and/or RIPA (anti-gag and anti-env specificities), or even PCR which makes specific diagnosis of HTLV1/2. --Or if possible directly by PCR which has helped some authors to find provirus in seronegative people. Coinfections caused by HIV and by Strongyloides are the best documented. As a rule, HTLV1 seems to have rather a worsening effect on evolutiveness and on seriousness of the clinical picture caused by mixed infections, than the contrary (possibly for lack of experience and owing to slow evolution of HTLV1 pathology). Several mechanisms have been proposed concerning coinfections with HTLV1 and HIV (in vitro studies). --Immortalization of CD4 lymphocytes infected with HTLV1 by stimulating both IL2 and its receptor, and by activating lymphocytes with translocation of the replicating factor NF k B in the nucleus, on a promoting sequence of HIV-LTR by stimulating its replication. --The product of HTLV1 tax gene would also have a transactivating effect on the provirus HIV-LTR replication. And finally infection with HTLV1 may facilitate HIV by inducing CD4, molecule expression in non-expressing cells. In Strongyloides modulating effects of HTLV1 on the immune response would facilitate and predispose Strongyloides stercoralis multiplication. As far as other coinfections are concerned (caused by viruses, by parasites: such as malaria, filariasis, trypanosomiasis or by bacteria), epidemiological convergence (risk factors, and geographic distribution) on the one hand, and immunological dysregulation induced by the other, on the other hand, would be of varying importance. In conclusion, these data ask more questions than they answer. But it seems to be established that detection of HIV and Strongyloides should performed in every case HTLV1 carries and vice versa.

Blotting, Western↗
PubMed1992

HBV and HCV infection in i.v. drug addicts; coinfection with HIV.

A group of 122 drug addict patients were studied to evaluate the incidence of HIV, HBV, HCV infections and of laboratory findings of hepatic damage. Our data show that hepatic damage is more frequent in patients affected by HBV-HCV coinfection than those with HBV or HCV infection alone and that HIV positivity supports HBV-HCV coinfection.

Adolescent↗
PubMed1979

Synthesis of a small RNA in cells coinfected by standard and defective interfering particles of vesicular stomatitis virus.

A small RNA, containing approximately 50 nucleotides, is synthesized by cells coinfected with standard vesicular stomatitis virus and its defective interfering (DI) particles. Infection of cells by standard virus or DI particles alone does not lead to synthesis of significant amounts of small RNA. The RNA is initiated at its 5' end with (p)ppXp and is not polyadenylylated at the 3' end despite a content of 51% adenosine. It has sequences complementary to the genome of a DI particle. The synthesis of the small RNA correlates with the replication of the genome of DI particles with molar ratio small RNA/genome RNA of DI particles greater than 50. When replication of DI genomes is prevented by the addition of cycloheximide or prior UV irradiation of DI particles, small RNA is not synthesized in coinfected cells. These results indicate that the small RNA is not the result of transcriptional initiation and that it may relate to interference mediated by DI particles.

Animals↗
PubMed1992

Coinfection with multiple strains of the Epstein-Barr virus in human immunodeficiency virus-associated hairy leukoplakia.

Epstein-Barr virus DNA was analyzed from specimens of hairy leukoplakia, an oral lesion that occurs in patients infected with the human immunodeficiency virus. The simultaneous presence of both type 1 and type 2 Epstein-Barr virus was demonstrated by Southern blot analysis and polymerase chain reaction assay. Restriction fragment length polymorphisms in the BamHI WYH region and in clones of the EcoRI C region suggested the presence of multiple strains of type 1 and type 2 viruses. The demonstration of multiple variably sized BamHI H fragments on Southern blot analysis and cloning of the EBNA-2 gene coding region also suggested the presence of multiple viral strains or variants coinfecting hairy leukoplakia. Recombination of the viral genome in and around the EBNA-2 gene apparently generated viral variants that replicated efficiently, one of which appeared to increase in abundance in a lesion over time. These data indicate that hairy leukoplakia involves coinfection with multiple strains of replicating Epstein-Barr virus and the endogenous generation of viral variants, some of which have mutations of the EBNA-2 gene.

Antigens, Viral↗
PubMedDate not supplied

Primary B cell lymphoma of the rectum in a patient coinfected with HIV-1 and HTLV-I.

This report describes a clinical case of a large cell, immunoblastic plasmacytoid malignant B-cell lymphoma of the rectum in an AIDS patient coinfected with HTLV-I. The malignant cells showed clonal genetic rearrangement of the HC (JH) and LCK genes. Infection by EBV was demonstrated serologically and with slot blots using genomic DNA of the cancer cells. Southern blot analysis with DNA extracted from the lymphoma cells were negative for HTLV-I. The patient received seven cycles of VACO-B which induced complete but transient clinical remission of the tumor. The final outcome of the patient is unknown.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Modulatory effects of Epstein-Barr, herpes simplex, and human herpes-6 viral infections and coinfections on cytokine synthesis. A comparative study.

Herpesviruses such as EBV, HSV, and human herpes virus-6 (HHV-6) have a marked tropism for cells of the immune system and therefore infection by these viruses may result in alterations of immune functions, leading at times to a state of immunosuppression. We report the results of a comparative study in which we found that EBV, HSV-1, and HHV-6 act differentially on the immune system with regard to their effect on the synthesis of IL-1 beta, IL-6, and TNF-alpha, i.e., three immunoregulatory cytokines mainly secreted by activated monocytes/macrophages. Using the polymerase chain reaction technique, analyses of the mRNA levels for each of the three monokines after viral infection indicated that the effect exerted by each of these herpesviruses on cytokine synthesis by human PBMC was detectable at the transcriptional level. Different amounts of IL-1 beta protein were detected in infected PBMC cultures, HHV-6 being the strongest IL-1 beta up-regulatory among these three herpesviruses. Spontaneous releases of IL-6 and TNF-alpha were found reduced after infection by HHV-6 and EBV, respectively. In comparison to EBV and HHV-6, HSV-1 proved to be a weak monokine enhancer. Results of coinfection studies indicated that virus-induced suppressive effects on cytokine synthesis are dominant. In fact, EBV inhibited TNF-alpha synthesis even in the presence of HHV-6, a strong up-regulator of TNF-alpha synthesis. Similarly, EBV was unable to stimulate IL-6 production in the presence of HHV-6. Viral structural component(s) appeared to be responsible for the up-regulation of IL-6 by both EBV and HSV-1, and of TNF-alpha by HSV-1. Taken together, our observations illustrate that herpesviruses can selectively regulate cytokine synthesis thereby disturbing immune homeostasis; this effect may favor pathogenic events, including the reactivation and/or spread of other infectious agents within the host.

Base Sequence↗
PubMed1991

Pneumonitis associated with coinfection by human herpesvirus 6 and Legionella in an immunocompetent adult.

The authors report a case of pneumonitis in a young healthy man caused by coinfection with human herpesvirus 6 (HHV-6) and Legionella pneumophila. The patient's course was complicated by severe respiratory, renal, hepatic, and central nervous system dysfunctions, which were believed to be primarily the results of his Legionella infection. Aggressive antibiotic treatment produced no response, and Legionella remained isolatable from lung tissue throughout several weeks of antimicrobial therapy. Human herpesvirus 6 was isolated from a sample of peripheral blood during the acute stage of the patient's illness, and numerous HHV-6--infected macrophages and lymphocytes were detected by immunohistochemical staining of biopsy-derived lung tissue. Paradoxically treatment of the patient with high-dose corticosteroids resulted in dramatic improvement of his condition, including clearance of the Legionella infection. The demonstration that corticosteroids efficiently inhibit HHV-6 replication in vitro suggests that the virus may have contributed to the patient's pneumonitis by enhancing tissue inflammation, by compromising the function of pulmonary macrophages, and, perhaps, by destroying the patient's CD4+ T lymphocytes. Human herpesvirus 6 may be able to function as a synergistic cofactor in lung infections by Legionella and other pathogens.

Adrenal Cortex Hormones↗
PubMed1991

Induction by some protein kinase inhibitors of differentiation of a mouse megakaryoblastic cell line established by coinfection with Abelson murine leukemia virus and recombinant SV40 retrovirus.

Mouse C1 line cells are megakaryoblastic cells established by coinfection of Abelson murine leukemia virus and recombinant simian virus 40. We examined the effects of various compounds on growth and differentiation of these cells. Megakaryocytic differentiation of C1 cells was not induced by cytokines that stimulate megakaryocytic maturation of normal progenitor cells, such as interleukin 3 and 6 and granulocyte-macrophage colony-stimulating factor. However, the cells were induced to differentiate into megakaryocytes by treatment with some protein kinase inhibitors. The inhibition of v-abl tyrosine kinase activity preceded induction of differentiation of the cells treated with tyrosine kinase inhibitors such as genistein, herbimycin A, and erbstatin. Treatment of C1 cells with a v-abl antisense oligomer inhibited their proliferation and induced acetylcholinesterase activity, a typical marker of megakaryocytic differentiation. These results suggest that inhibition of v-abl function is associated with induction of megakaryocytic differentiation of C1 cells. Among the compounds tested, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), a potent inhibitor of cyclic nucleotide-dependent and Ca(2+)-phospholipid-dependent (protein kinase C) protein kinases, was the most potent inducer of differentiation of C1 cells. However, the differentiation-inducing effect of H-7 was unlikely to be mediated through inhibition of protein kinase C or cyclic nucleotide-dependent kinases, because other types of inhibitors of these kinases were not effective, and a protein kinase activator (phorbol ester) induced differentiation of C1 cells. Moreover, neither v-abl mRNA expression nor v-abl kinase activity in C1 cells was affected by treatment with H-7. These findings indicate that induction of megakaryocytic differentiation by H-7 is not related to inhibition of v-abl kinase, but rather to some novel function of H-7.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1978

Coinfection with a rhabdovirus: vesicular stomatitis virus of Indiana and New-Jersey serotypes.

Coinfection of cells with vesicular stomatitis virus (VSV) of Indiana and New-Jersey serotypes were performed. Thermosensitive mutants (ts) of VSV Indiana and the wild type strain (+) of New-Jersey were used. Harvests and titrations were made at permissive(PT) and nonpermissive (NPT) temperatures. It was shown that the harvest was mainly composed of one parental-like infectious particles. The dominance of one serotype over the other was shown to be a function of the relative multiplicity of the two viruses; the presence of a thermosensitive lesion imparts a disadvantage to the corresponding serotype. Non parental-like particles were also detected. As expected, these particles were detected only in two conditions. 1) Harvest performed at NPT and titrations allowed at PT.- Most of the infectious particles (i.e. twin particles) resistant to anti-Nj serum developped a plaque (i.e. mixed-plaque)containing virions of both serotypes: Indiana (ts) and New-Jersey (+). After sonication or EDTA treatment of the harvest, prior to titrations, no more mixed-plaques were formed. Examination of the harvest by electron microscopy showed that 7-17 % of the particles formed aggregates; therefore, it is likely that the twin-particles are in fact aggregates. 2) Harvest performed at PT and titrations allowed at NPT.-It has been shown that 1 % of the wild type infectious particles was resistant to anti-Nj serum even though being of Nj genotype. It was inactivated by a mixture of anti-Nj and anti-In sera and therfore behave as pseudotypes. But since twin particles, when plated at Nt, would give rise to an homogenous progeny from New-Jersey (+), they could be confused with pseudotypes. Under those conditions there is no absolute evidence that phenotypic mixing really occurs between VSV of Indiana and New-Jersey serotypes.

Cell Line↗
PubMed2026

STRONGYLID COINFECTIONS IN SYMPATRIC CHIMPANZEES AND GORILLAS FROM THE REPUBLIC OF THE CONGO REVEALED BY FECAL METAGENOMICS.

Soil-transmitted strongylid nematodes are common intestinal parasites of African great apes, yet most surveys have relied on microscopy or targeted PCR assays that are limited in taxonomic breadth and comparability across hosts. I reanalyzed 46 publicly available shotgun fecal metagenomes from sympatric central chimpanzees (Pan troglodytes troglodytes; n = 18) and western lowland gorillas (Gorilla gorilla gorilla; n = 28) in the Goualougo Triangle, Nouabal&#xe9;-Ndoki National Park, Republic of the Congo, to test whether host species structures genus-level strongylid community composition and relative read signal. Non-host reads were classified against a custom strongylid-focused database targeting 4 genera repeatedly reported from African apes: Ancylostoma, Necator, Oesophagostomum, and Trichostrongylus. All 4 focal genera were detected in every library under baseline filtering, and multi-genus detection remained robust under increasingly stringent read-count thresholds. However, host species differed strongly in community composition. Chimpanzee libraries had relatively even genus-level profiles, whereas gorilla libraries were consistently Necator-dominated. Gorillas also had substantially higher relative strongylid read abundance. The results show that shotgun metagenomic reanalysis can recover host-structured strongylid community signals from wildlife samples and can complement targeted parasitological surveys in conservation and One Health surveillance.

Animals↗