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At least 163 records · Page 9Linked to original sources
PubMed1992

[Acute viral hepatitis: pathogenesis and clinical manifestations].

This is a review of several mechanisms in the acute and chronic progress of viral hepatitis. Investigation of these mechanisms may have an important role in the diagnosis and treatment of chronic hepatitis. Clinical features of acute non-A, non-B hepatitis were studied in 110 patients. Most of the patients had a surgical intervention or/and received blood transfusion previously. The clinical course of the cases was very mild and most of the patients have the cholestatic form of the disease. A 39% anti-HCV antibody seropositivity rate was seen in these cases.

Acute Disease↗
PubMedDate not supplied

Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted.

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.

Animals↗
PubMed2005

Recurrent respiratory papillomatosis: pathogenesis to treatment.

PURPOSE OF REVIEW: Recurrent respiratory papillomatosis remains a serious disease and is commonly treated by otolaryngologists. The goals of this review are to update physicians on current understandings regarding viral pathogenesis, patient risks, and current trends in treatment strategies. RECENT FINDINGS: Surgical debulking still remains the foundation of treatment; however, newer surgical approaches utilizing microdebriders are replacing laser ablation. Genetic studies have identified individuals with specific immune cell alleles to be at greater risk for persistent infection. Our understanding of the viral pathogenesis has increased by the identification of a viral mechanism to downregulate antigen expression in cells infected with human papillomavirus, thus possibly allowing decreased immune detection. Although the viral types responsible for recurrent respiratory papillomatosis have been identified, the mechanism by which they alter cellular growth has not been identified. Research studies investigating adjuvant medical therapies aimed at reducing required surgical therapy intervals and possibly helping cure the infection are being completed. A safe, effective adjuvant therapy is still currently not available. SUMMARY: Improved surgical approaches have slightly enhanced patient care; however, more research is needed to understand how human papillomavirus causes disease so that these therapies can be developed.

Antineoplastic Agents↗
PubMedDate not supplied

Sequence of reovirus haemagglutinin predicts a coiled-coil structure.

The use of modern techniques has led to new insights into the molecular mechanisms of viral pathogenesis. Although the infectious process is quite complex, it is clear that one critical stage, the interaction of viral attachment proteins with cell-surface receptors, often has a major role in determining the pattern of infection. The mammalian reoviruses have served as useful models for understanding the molecular basis of viral pathogenesis. The mammalian reovirus haemagglutinin (sigma 1 protein), which is an outer capsid protein, has been shown to be a major factor in determining virus-host cell interactions. To further our understanding of the structure and function of the haemagglutinin, we have cloned a complementary DNA copy of the reovirus type 3 S1 double-stranded RNA gene which encodes the virus haemagglutinin and have sequenced the DNA complementary to the S1 gene. Analysis of the predicted amino-acid sequence of the virus haemagglutinin has allowed us to determine that the amino-terminal portion contains an alpha-helical coiled-coil structure and that the carboxy-terminal portion contains the receptor-interacting domains. Using this information, we propose here a model of how the reovirus haemagglutinin is attached to the virus particle.

Amino Acid Sequence↗
PubMed2006

Role of protein modifications mediated by transglutaminase 2 in human viral diseases.

Transglutaminase 2 (TG2) belongs to a family of calcium-dependent enzymes that catalyze transamidation reaction, producing polymerized, polyaminated or deamidated proteins. Recently, a growing number of viral proteins as well as cellular proteins with which they interact have been found to be modified by TG2, suggesting a novel function for TG2 in viral pathogenesis. This review summarizes the results of relevant research, examines the mechanisms underlying TG2 function in host-virus interactions and proposes a model for viral pathogenesis involving TG2.

Animals↗
PubMed2002

Functional conservation of HIV-1 Vpr and variability in a mother-child pair of long-term non-progressors.

Increasing evidence suggests that HIV-1 Vpr is required in vivo for viral pathogenesis. Since Vpr displays multiple activities, little is known about which Vpr-specific activities are conserved in naturally occurring viruses or how natural mutations in Vpr might modulate viral pathogenesis in HIV-infected individuals. The goals of this study were to evaluate the functional variability of Vpr in naturally occurring viruses. The Vpr-specific activities of nuclear localization, induction of cell cycle G2 arrest and cell death were compared between viruses isolated from the fast progressing AIDS patients and a mother-child pair of long-term non-progressors (LTNPs). Wild-type Vpr activities were found in all of the viruses that were isolated from the fast progressing AIDS patients except for the truncated Vpr(IIIB) which lacked these activities. In contrast, defective Vpr were readily detected in viral populations isolated, over an 11-year period, from the mother-child pair. Sequence analyses indicated that these Vpr carried unique amino acid substitutions that frequently interrupted a highly conserved domain containing an N-terminal alpha-helix-turn-alpha-helix. Thus, Vpr activities are generally conserved in naturally occurring viruses. The functionally defective Vpr identified in the mother-child pair of LTNPs are likely to be unique and may possibly contribute to the slow disease progression.

Adolescent↗
PubMed2006

Co-infection by Semliki forest virus and malarial parasite modulates viral multipucation, pathogenesis and cytokines in mice.

Environmental, technological and societal factors continue to have a dramatic effect on infectious diseases worldwide and are considered to be facilitating the emergence of several infectious diseases at a time. Co-infection with different species of viral and malaria infections are currently emerging problems of dual infection in the developing as well as developed countries. Understanding of interactions between the host, malaria and virus infection is of current concern and we have initiated studies to delineate the mechanisms involved during the progression of Semliki forest virus (SFV) and Plasmodium yoelii (P. yoelii) infection in mice. Enhanced virus multiplication and up-regulation of cytokine mRNA level in P. yoelii and SFV co-infected mice were observed on day 4 post-infection compared to respective controls. Collectively, our observations indicate that malaria infection may influence virus multiplication, pathogenesis and up-regulation of cytokine mRNA during co-infection in mice.

Alphavirus Infections↗
PubMed2000

Vaccination with tat toxoid attenuates disease in simian/HIV-challenged macaques.

The Tat protein is essential for HIV type 1 (HIV-1) replication and may be an important virulence factor in vivo. We studied the role of Tat in viral pathogenesis by immunizing rhesus macaques with chemically inactivated Tat toxoid and challenging these animals by intrarectal inoculation with the simian/human immunodeficiency virus 89.6PD. Immune animals had significantly attenuated disease with lowered viral RNA, interferon-alpha, and chemokine receptor expression (CXCR4 and CCR5) on CD4(+) T cells; these features of infection have been linked to in vitro effects of Tat and respond similarly to extracellular Tat protein produced during infection. Immunization with Tat toxoid inhibits key steps in viral pathogenesis and should be included in therapeutic or preventive HIV-1 vaccines.

Animals↗
PubMed1995

[Vasculitis of viral origin. Pathogenesis and therapeutic implications].

Some viruses are unquestionably the cause of vasculitis, by different mechanisms: circulating immune complexes, cryoglobulinemia and/or direct infection of the blood vessel. The main viruses responsible for vasculitis are hepatitis B & C viruses, cytomegalovirus, parvovirus B19 and human immunodeficiency virus. Viral vasculitis are clinically protean, most of the time similar to idiopathic vasculitis. The manifestations due to the virus itself are sometimes hidden and vasculitis may reveal the viral infection. In some cases of viral vasculitis, particularly in hepatitis virus-induced vasculitis, antiviral therapy may help in controlling the disease. A viral etiology must be considered during atypical vasculitis.

Cytomegalovirus Infections↗
PubMed2002

[Involvement of immune system in the pathogenesis of viral myocarditis].

Myocarditis is thought to be commonly caused by various viruses, and accumulating evidence links viral myocarditis with the eventual development of dilated cardiomyopathy. Heart disease is the most prevalent cause of morbidity and mortality in developed countries. Cytokines are being increasingly recognized as an important factor in the pathogenesis of myocarditis and cardiomyopathy. Elevated levels of circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. A number of reports have shown that cytokines generated by activated immune cells cause an increase in nitric oxide (NO) via induction of NO synthase. Increased generation of NO may induce myocardial damage. It has been suggested that NO can be either beneficial or harmful to the host, NO can protect the myocardium against damage from CVB3 infection by inhibiting viral replication. A better molecular understanding of the direct effect of viral infection on cardiac myocytes and the balance of beneficial and detrimental effects of the immune response will ultimately provide insight into the mechanisms by which viral infections cause cardiomyopathy in humans.

Animals↗
PubMed2004

HIV accessory proteins and surviving the host cell.

Human immunodeficiency virus generates the accessory proteins Nef, viral infectivity factor (Vif), viral protein R, and viral protein U or viral protein X during viral replication in host cells. Although the significance of these accessory proteins is often lost in vitro, they are essential for viral pathogenesis in vivo. Therefore, these proteins have much potential as antiviral targets. Recent data reveal Vif perturbs an ill-defined antiviral pathway in host cells allowing HIV replication. These data highlight a common feature among HIV accessory proteins in manipulating the host to aid viral pathogenesis. Therefore, these new insights into Vif and other HIV accessory proteins are reviewed, emphasizing host cell interactions and new targets for therapeutic intervention.

HIV Infections↗
PubMed1994

Antibody-dependent enhancement of infection and the pathogenesis of viral disease.

Antibody-dependent enhancement of infection (ADE) is an in vitro serological phenomenon--or a group of phenomena--in which viral infection of susceptible cells is modified by the addition of virus-reactive antibody. Evidence suggests that ADE reflects immunologic processes that occur in vivo. Various severe and even fatal viral conditions of humans and animals, including dengue shock syndrome, the "early-death phenomenon" in experimental infections of immune animals, and other vaccine- and immunoglobulin-modified conditions, have been attributed to ADE by some researchers. ADE has caused great concern in relation to the development of vaccines against dengue virus and human immunodeficiency virus. More data are urgently needed on the mechanisms and determinants of ADE and on its alleged role in disease pathogenesis and in vaccine-associated phenomena.

Age Factors↗
PubMed1998

Characterization of two avian reoviruses that exhibit strain-specific quantitative differences in their syncytium-inducing and pathogenic capabilities.

We previously proposed that the conservation of the nonessential syncytium-inducing phenotype among all reported avian reovirus (ARV) isolates may reflect a mechanism for enhanced virus dissemination in vivo, which in turn could contribute to the natural pathogenicity of ARV. Direct testing of this hypothesis has been hampered by the lack of available virus strains with defined differences in their fusion-inducing capability. We now report on the characterization of two ARV strains, ARV-176 and ARV-138, that exhibited strain-specific differences in their fusogenic properties, which correlated with their pathogenic potential in embryonated eggs. Moreover, both virus strains possessed similar replicative abilities in cell culture, suggesting that the weakly fusogenic ARV-138 virus is specifically inhibited in its syncytium-inducing ability. To test the use of these viruses for reassortant studies aimed at assessing the role of cell fusion in viral pathogenesis, a preliminary genetic analysis was undertaken using a monoreassortant that contained nine genome segments from the parental ARV-138 virus and the S1 genome segment from the highly fusogenic and pathogenic ARV-176 parental virus. The monoreassortant possessed the full fusogenic potential of the ARV-176 parental virus and displayed enhanced embryo pathogenicity, providing the first genetic evidence implicating the ARV S1 genome segment in both syncytium formation and viral pathogenesis.

Animals↗
PubMed1990

Reovirus-induced liver disease in severe combined immunodeficient (SCID) mice. A model for the study of viral infection, pathogenesis, and clearance.

Adult severe combined immunodeficient (SCID) mice can be infected by the oral route with reovirus, and a systemic infection can be established. Infectious virus is recovered from all internal organs, and the mice die in 4-6 wk. Chronic, discrete inflammatory lesions appear in the liver of infected mice, and are associated with hepatocytes containing demonstrable levels of viral antigen. The adoptive transfer of Peyer's patch (PP) cells from congenic mice before infection protects the SCID mice against disease and death. Immune donor PP cells can be distinguished from nonimmune cells by their ability to contain and resolve infection by 1 wk after challenge.

Animals↗
PubMed1998

The R33 G protein-coupled receptor gene of rat cytomegalovirus plays an essential role in the pathogenesis of viral infection.

We have identified a rat cytomegalovirus (RCMV) gene that encodes a G-protein-coupled receptor (GCR) homolog. This gene (R33) belongs to a family that includes the human cytomegalovirus UL33 gene. R33 was found to be transcribed during the late phase of RCMV infection in rat embryo fibroblasts. Unlike the mRNAs from all the other members of the UL33 family that have been studied to date, the R33 mRNA is not spliced. To study the function of the R33 gene, we constructed an RCMV strain in which the R33 open reading frame is disrupted. The mutant strain (RCMV deltaR33) did not show differences in replication from wild-type RCMV upon infection of several rat cell types in vitro. However, marked differences were seen between the mutant and wild-type strain in the pathogenesis of infection in immunocompromised rats. First, the mutant strain induced a significantly lower mortality than the wild-type virus did. Second, in contrast to wild-type RCMV, the mutant strain did not efficiently replicate in the salivary gland epithelial cells of immunocompromised rats. Although viral DNA was detected in salivary glands of RCMV deltaR33-infected rats up to 14 days postinfection, it could not be detected at later time points. This indicates that although the strain with R33 deleted is probably transported to the salivary glands in a similar fashion to that for wild-type virus, the mutant virus is not able to either enter or replicate in salivary gland epithelial cells. We conclude that the RCMV R33 gene plays a vital role in the pathogenesis of infection.

Amino Acid Sequence↗
PubMed2006

Evolving role of leukotrienes in the pathogenesis of viral infections, including otitis media.

Otitis media (OM) is one of the most common childhood disorders and has been associated with an alarming rise in prevalence. Because medical therapy with antibiotics, antihistamines, decongestants, and corticosteroids has no demonstrable efficacy in the treatment of OM, the mainstay of treatment is surgical intervention. Although effective, surgical treatment is quite expensive and exposes patients to the risks associated with general anesthesia. Results of recent studies suggest that locally produced leukotrienes may play a role in the pathogenesis of OM. As such, a potential candidate for treatment of OM is the leukotriene receptor antagonist, montelukast, which has been approved by the US Food and Drug Administration for the treatment of asthma and/or allergic rhinitis. If proven effective, this drug's safety/convenience profiles and indication for children as young as 6 months of age would make it suitable for treatment of OM, and perhaps even prophylaxis of OM in at-risk populations.

Acetates↗
PubMed2003

IL-13 is sufficient for respiratory syncytial virus G glycoprotein-induced eosinophilia after respiratory syncytial virus challenge.

Although well studied in settings of helminth infection and allergen sensitization, the combined contributions of IL-4 and IL-13 and their signaling pathways in models of viral pathogenesis have not been reported. Using a murine model of respiratory syncytial virus (RSV) infection, we evaluated the contribution of IL-13, alone and in conjunction with IL-4, during immunization with recombinant vaccinia virus expressing RSV G glycoprotein (vvGs) or with formalin-inactivated RSV (FI-RSV). We showed that both IL-4 and IL-13 activity must be inhibited to modulate G-specific responses resulting in severe RSV-induced disease. Inhibition of IL-4 or IL-13 activity alone had minimal impact on disease in vvGs-immunized mice. However, treatment of IL-4-deficient mice with IL-13Ra during vvGs immunization reduced IL-5, IL-13, and eotaxin production and pulmonary eosinophilia after RSV challenge. In contrast, FI-RSV-induced immune responses were diminished when either IL-4 or IL-13 activity was blocked. After RSV challenge, these type 2 T cell responses were also diminished in vvGs-primed IL-4Ralpha-deficient mice. Our data suggest that secreted vvGs uses mechanisms requiring signaling through the IL-4Ralpha-chain by either IL-4 or IL-13 for induction of eosinophilia and is the first description of the relative contributions of IL-4, IL-13, and their receptors in viral pathogenesis.

Animals↗
PubMed1992

Mouse cytomegalovirus infection induces antibodies which cross-react with virus and cardiac myosin: a model for the study of molecular mimicry in the pathogenesis of viral myocarditis.

Mouse cytomegalovirus (MCMV) infection induces persisting myocarditis in the susceptible BALB/c strain. Autoantibodies to cardiac myosin are produced in both susceptible BALB/c and resistant C57BL/6 mice following MCMV infection. These affinity-purified anti-cardiac myosin antibodies cross-react with MCMV protein(s). The polypeptides of CMV which share immunological cross-reactivity with the 200,000 MW polypeptide, the heavy chain of myosin, were viral polypeptides of 83,000, 94,000 and 116,000 MW recognized by BALB/c post-infection sera and polypeptides of 66,000 and 94,000 MW recognized by C57BL/6 post-infection sera. Passive transfer of anti-cardiac myosin antibodies from Day 56 post-infection sera of the BALB/c strain induced inflammation and necrosis of the myocardium of uninfected BALB/c recipients. This late immune sera contains autoantibodies specific for the cardiac isoform of myosin. Furthermore, immunization with cardiac myosin induced myocarditis and high titres of cardiac myosin antibodies in uninfected mice of the susceptible BALB/c strain only. However, antibodies to myosin elicited in cardiac myosin-immunized BALB/c mice did not cross-react with MCMV by ELISA. We suggest that virus infection may modulate the immune recognition of the common-epitope(s) shared between MCMV protein(s) and the heavy chain of myosin. Of particular interest is the possibility that molecular mimicry of CMV with cardiac myosin may contribute to the pathogenesis of autoimmune myocarditis following virus infection.

Animals↗