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PubMed2001

Apoptosis in viral hepatitis B and C.

Tumor necrosis factor (TNF) and TNF receptors (TNFR) are members of the growing TNF ligand and receptor families known to be involved in apoptosis, viral pathogenesis and immune regulation. The present report will focus on the role of apoptosis in the pathogenesis of viral hepatitis B and C. Although TNF was reported years ago to modulate viral infections, recent findings on the molecular pathways involved in TNFR signaling have allowed a better understanding of the molecular interactions between cellular and viral factors within the infected cell. The interactions of viral proteins with intracellular components downstream of the TNFR have highlighted at the molecular level that viruses can manipulate the cellular machinery to escape the immune surveillance and to favor spread infection. We will review here the mechanism of apoptosis and the role of viral proteins that regulate apoptosis in viral hepatitis B and C.

Apoptosis↗

PubMed1996

Reovirus infection in rat lungs as a model to study the pathogenesis of viral pneumonia.

We undertook the present study to elucidate the pathogenesis of the pathologic response to reovirus infection in the lungs and further understand the interactions of reoviruses with pulmonary cells. We found that reoviruses were capable of causing acute pneumonia in 25- to 28-day-old Sprague-Dawley rats following intratracheal inoculation with the reoviruses type 1 Lang (T1L) and type 3 Dearing (T3D). The onset of the pneumonia was rapid, marked by type I alveolar epithelial cell degeneration, type II alveolar epithelial cell hyperplasia, and the infiltration of leukocytes into the alveolar spaces. More neutrophils were recruited into the lungs during T3D infection than during T1L infection, and the serotype difference in the neutrophil response was mapped to the S1 gene of reovirus. Viral replication in the lungs was required for the development of pneumonia due to T1L and T3D infections, and replication occurred in type I alveolar epithelial cells. T1L grew to higher titers in the lungs than did either T3D or type 3 clone 9, and the S1 gene was found to play a role in determining the level of viral replication. We propose that experimental reovirus infection in the lungs can serve as a model for the pathogenesis of viral pneumonia in which pulmonary inflammation results following direct infection of lung epithelial cells.

Animals↗

PubMed2004

Semliki forest virus infection of laboratory mice: a model to study the pathogenesis of viral encephalitis.

Semliki Forest virus (SFV) infection of the laboratory mouse provides an experimental system to study the pathogenesis of viral encephalitis. Following extraneural inoculation the virus is efficiently neuroinvasive and crosses the blood-brain barrier to initiate perivascular foci of infection in neurons and oligodendrocytes. The outcome of infection ranges from clinically unapparent mild encephalitis to fatal panencephalitis. SFV infections of the developing nervous system are always highly destructive and are generally fatal. In contrast, SFV infections of the mature nervous system can result in persistent infection with no apparent cell loss. This dramatic difference is attributable to developmental changes in the interactions between virus and CNS cells. Antibody responses clear the systemic infection and control the CNS infection. CD8+ T-cells are required to generate the lesions of inflammatory demyelination which can be a feature of the neuropathology. This article reviews the pathogenesis of SFV encephalitis, describing the neuropathology and the mechanisms which underlie it and which may be fundamental to many viral encephalitides.

Alphavirus Infections↗

PubMed1997

Rapid evolution of viral RNA genomes.

Mutation rates during RNA virus replication are several orders of magnitude larger than those operating during replication of cellular DNA. This results in the continuous generation of mutant genomes and in their rating in competition with other variants present and arising in the population. The dynamic mutant distributions that constitute RNA virus populations are termed quasispecies. This concept has facilitated links between population genetics and virology and has a number of important implications for viral pathogenesis and the control of viral disease. One of them is that the mutant spectra in RNA viruses constitute large reservoirs of genetic and phenotypic variants with potentially altered biological properties. Individual mutants kept in a low proportion under a set of environmental conditions may become dominant following an environmental change. Relevant to this review are possible links between the alteration of quasispecies distributions and nutritional deficiencies and oxidative stress in cells. In addition to being a possible mechanism of viral pathogenesis, oxidative stress, and other environmental modifications resulting from nutritional imbalances, may promote population disequilibrium in replicating viruses. In particular, the increased mutagenesis mediated by oxidative DNA damage could also affect replicating RNA and integrated provirus, extending the mutant repertoire of viruses. Also, the impairment of humoral and cellular immune functions may delay or prevent viral clearance, leading to an expanded representation of viral mutants in the infected organism. Thus, nutritional deficiencies are a potential source of viral mutants with altered biological properties.

Biological Evolution↗

PubMed1986

Pathogenesis of viral infections.

The article considers factors that influence pathogenesis, initiation of infection, dissemination of virus within a host, lytic viral infections, viral immunosuppression, viral immunopathology, and viral oncogenesis.

Animals↗

PubMed2003

Pathogenesis of neurotropic herpesviruses: role of viral glycoproteins in neuroinvasion and transneuronal spread.

Neuroinvasion by herpesviruses requires entry into nerve endings in the periphery, transport to the cell body, replication in the cell body, axonal transport to the synapse and transneuronal viral spread. Entry occurs after receptor binding by fusion of virion envelope and cellular plasma membrane followed by microtubuli-assisted transport of capsids to the nuclear pore. By transneuronal spread, the virus gains access to synaptically linked neuronal circuits. A common set of herpesvirus glycoproteins is involved in entry and direct viral cell-cell spread. However, both processes can be distinguished by involvement of additional viral components. Interestingly, transneuronal spread appears to be functionally linked to intracytoplasmic formation of mature virions. This review will focus on the importance of herpesvirus envelope glycoproteins for infection of neurons and transneuronal spread, and their influence on viral pathogenesis.

Animals↗

PubMed2000

[The role of intercellular adhesion molecule-1/lymphocyte function-associated antigen-1 in the pathogenesis of viral hepatitis B].

OBJECTIVE: To study the role of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in the pathogenesis of viral hepatitis B. METHODS: ICAM-1, LFA-1 and CD(8) expression in the livers of 11 healthy persons and 70 patients with HBV infection were studied by using immunohistochemical techniques. Hepatic coexpression of ICAM-1 and LFA-1 were studied using double staining immunohistochemical techniques. RESULTS: In the areas of inflammation and necrosis, intensive infiltration of LFA-1 positive lymphocytes were often observed around hepatocytes with enhanced ICAM-1 expression, with some of these lymphocytes in close contact with hepatocytes expressing ICAM-1. In addition, the debris of necrotic cells and injured hepatocytes were found at the surrounding of LFA-1 positive lymphocytes. CONCLUSION: The interaction of ICAM-1 and LFA-1 is involved in mediating the adhesion of lymphocytes and hepatocytes, and it plays an important part in the immunopathogenesis of chronic viral hepatitis B and severe viral hepatitis B.

Adult↗

PubMed2002

Realities and enigmas of human viral influenza: pathogenesis, epidemiology and control.

Influenza A is a viral disease of global dimension, presenting with high morbidity and mortality in annual epidemics, and in pandemics which are of infrequent occurrence but which have very high attack rates. Influenza probes reveal a continuing battle for survival between host and parasite in which the host population updates the specificity of its pool of humoral immunity by contact with and response to infection with the most recent viruses which possess altered antigenic specificity in their hemagglutinin (HA) ligand. HA ligand binds the virus to the cell to bring about infection. Viral survival relies on escape from host immunity through antigenic alterations in nature which arise through genetic drift by point mutation principally of the HA gene, or through genetic shift by reassortment exchange of the HA ligand with that of viruses retained in avian species. Partial control of influenza is by use of killed whole, subunit, or possible live virus vaccines, all of which rely on worldwide surveillance to provide early detection of the altered immunologic specificity of the next virus to come. Future global surveillance may be aided by studies of sampled viral isolates in laboratories having capabilities for accelerated genetic sequencing and for automated rapid throughput analyses as well. Influenza vaccines of the future must be directed toward use of conserved group-specific viral antigens, such as are present in transitional proteins which are exposed during the fusion of virus to the host cell. Chemotherapy, though still primordial, must eventually provide the ultimate solution to vaccine failures. Probing the enigma of the severe influenza pandemic of 1918-1919 is an exciting contemporary venture in which genetic reconstruction of the viral genome from surviving archival RNA is being conducted with great success. Present evidence reveals successive recycling in pandemics, of only 3 of the 15 possible avian viral HAs. Pandemics are believed, conventionally, to be derived solely by rare events in which wild viruses of man acquire a new HA ligand of avian origin. There might be an alternative possibility involving a periodicity in selective control by the host population itself, in its receptivity or rejection at a particular time of particular reassortant viruses which might be created more frequently in nature than we are presently aware. This hypothesis, though remote, provides a different way to view and to probe the enigma of pandemic influenza.

Adolescent↗

PubMed2000

Molecular pathogenesis of viral hepatitis.

The global burden of chronic liver disease caused by persistent infection with hepatitis B and C viruses has meant the urgent development of therapeutic strategies designed to control active replication and therefore prevent subsequent clinical sequelae. Advances in these therapeutic strategies are now clearly happening, mainly as a consequence of a better understanding of the viral life cycle and the unique pathogenesis of each disease. Further progress should continue as further insights into the virus-cell relationship are derived, which will sharpen attention on specific viral targets as well as shift and enhance host cytokine responses.

Antiviral Agents↗

PubMed1997

[Pathology and pathogenesis of viral hepatitis].

Several factors viral genotype, mutations, vírus-host interaction, expression of viral proteins and host immune-reaction are very important in the pathogenesis of hepatotrop viral infections. Activation of Fas/Fas ligand system occurs during hepatitis which is responsible for the apoptosis of vírus infected hepatocytes. The histological features in chronic hepatitis can be classified based on the activity of near inflammatory alterations ("grade"). Stage of chronic hepatitis describes the degree of fibrosis and architectural alterations.

Apoptosis↗

PubMedDate not supplied

Pathogenesis of viral hepatitis.

The aim of our research is to use animal models to elucidate the molecular basis for viral clearance and liver disease in the pathogenesis of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. The results herein discussed provide insight into immunological and virological processes that may lead to the development of new therapeutic strategies to terminate chronic HBV and HCV infections.

Animals↗

PubMed2001

Type I interferons and herpes simplex virus infection: a naked DNA approach as a therapeutic option?

Herpes simplex virus (HSV) types 1 and 2 are highly successful human pathogens that can elicit blinding herpetic keratoconjunctivitis, fatal sporadic encephalitis, aseptic meningitis, and increase the risk of acquiring additional sexually transmitted diseases. Type I interferons (IFN) play a significant role in controlling HSV pathogenesis by antagonizing viral replication and spread. Taking advantage of the susceptibility of HSV to IFNs, a novel approach of employing plasmid DNA cassettes expressing type 1 IFNs to antagonize viral pathogenesis has been undertaken. This review will describe recent work in our lab and those of others using naked DNA encoding cytokines to antagonize HSV replication and virus trafficking or immune-mediated pathogenesis as a result of viral assault to ocular tissue.

Animals↗

PubMed1983

Pathogenesis of viral encephalitis: demonstration of viral antigen(s) in the brain endothelium.

One of the enigmas in the pathogenesis of inflammation is why the white cells adhere to the endothelium. In trying to define the pathogenic mechanism, we carried out experiments on ferrets infected with an SSPE strain of measles virus. Using immunoperoxidase labeling techniques, viral antigens were demonstrated on the luminal surface and in the cytoplasm of endothelial cells, irrespective of the presence or absence of inflammatory changes. The degree of inflammation corresponded well with antibody titer. These data suggest that the viral antigen in the endothelial cells is the site of interaction between these cells and sensitized lymphoid cells.

Animals↗

PubMedDate not supplied

Apoptosis and pathogenesis of viral hepatitis C--an update.

Hepatitis C virus is a major causative agent of chronic liver disease. Viral genotype, mutations, virus-host interaction, expression of viral proteins and host immune-reaction are important factors in the pathogenesis of HCV infection. Precise pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remain unclear. Proposed mechanisms include direct viropathic effect, the host immune response mediated through cytotoxic T lymphocytes, both viropathic and cytopathic effects, and macrophages/monocytes. Apoptosis occurs both in acute or chronic hepatitis and has been suggested to be mediated through Fas antigen. In HCV infection, Fas expression is up-regulated in the liver cells in line with the severity of liver inflammation. When HCV-specific T cells migrate into hepatocytes and recognize the viral antigen via the T cell receptor, they become activated and express Fas ligand that transduces the apoptotic death signal to Fas-bearing hepatocytes resulting in their destruction. Thus, the Fas system plays an important role in liver cell injury by HCV infection. Possible inducers of apoptosis in hepatitis C include cytokines, especially tumor necrosis factor-alpha (TNF-alpha), released by inflammatory cells, and acting through TNF and other cytokine receptors.

Apoptosis↗

PubMed2005

Heat shock protein 40 is necessary for human immunodeficiency virus-1 Nef-mediated enhancement of viral gene expression and replication.

The human immunodeficiency virus-1 (HIV-1) Nef protein, originally identified as a negative factor, has now emerged as one of the most important viral proteins necessary for viral pathogenesis and disease progression. Nef has been also implicated in viral infectivity and replication, however, the molecular mechanism of Nef-induced viral gene expression and replication is not clearly understood. Although involvement of heat shock proteins in viral pathogenesis has been reported earlier, a clear understanding of their role remains to be elucidated. Here we report for the first time that Nef not only interacts with heat shock protein 40 (Hsp40) but it also induces the expression of Hsp40 in HIV-1-infected cells. The interaction between Nef and Hsp40 is important for increased Hsp40 translocation into the nucleus of infected cells, which seems to facilitate viral gene expression by becoming part of the cyclin-dependent kinase 9-associated transcription complex regulating long terminal repeat-mediated gene expression. The finding is consistent with the failure of the nef-deleted virus to induce Hsp40, resulting in reduced virus production. Our data further shows that, whereas, Hsp40 overexpression induces viral gene expression, silencing of Hsp40 reduces the gene expression in a Nef-dependent manner. Thus our results clearly indicate that Hsp40 is crucial for Nef-mediated enhancement of viral gene expression and replication.

Amino Acid Sequence↗

PubMed1992

Biologic response modifiers as antivirals in immunosuppressed hosts.

A wide variety of immunomodulators/biologic response modifiers (BRM) have been demonstrated to provide broad spectrum antiviral activity against both RNA and DNA viruses in several animal species. Dramatic decreases in mortality, reduced virus titers in tissues, and reduced histopathology can be produced. The antivirally effective agents include microbially derived materials, polyanions, cytokines, and chemically diverse small molecular weight chemicals. Antiviral efficacy with BRM treatment has been shown in numerous kinds of immunosuppression, emphasizing the potential for BRM treatment in immunocompromised patients. The greatest protective effects are observed with prophylactic or early therapeutic treatment. BRMs act indirectly, most likely by activating cells and/or inducing antiviral mediators early in the course of viral pathogenesis. In general, viral specific immune responses in BRM-treated and infected mice are absent or similar to those in untreated mice. Because BRMs are pleiotropic in their immunomodulatory effects, it has been difficult to establish whether one cell type or mediator is critical for the broad spectrum antiviral activity. Interferon appears to be critical for some small molecular weight synthetic compounds, but does not appear to explain all the antiviral activity of certain large molecular weight polyanions. Whether there is a unified antiviral mechanism among different BRMs remains to be determined.

Adjuvants, Immunologic↗

PubMed2005

Human herpesvirus 8--a novel human pathogen.

In 1994, Chang and Moore reported on the latest of the gammaherpesviruses to infect humans, human herpesvirus 8 (HHV-8). This novel herpesvirus has and continues to present challenges to define its scope of involvement in human disease. In this review, aspects of HHV-8 infection are discussed, such as, the human immune response, viral pathogenesis and transmission, viral disease entities, and the virus's epidemiology with an emphasis on HHV-8 diagnostics.

Antibody Formation↗

PubMed1989

Transgenic approach for the study of pathogenesis induced by human viruses.

An understanding of the pathogenesis of human viral diseases has been hampered by the lack of suitable animal models. However, with the advent in the last decade of transgenic technology, it is now possible to introduce one or more viral genes into the germ-line of animals. Thus, transgenic technology allows for the study of viral gene expression and function in the context of the whole animal. The focus of this review is to define the advantages and disadvantages of the transgenic approach in studies of viral pathogenesis. Studies involving a human DNA tumor virus (JCV) and a human retrovirus (HIV) will be described to illustrate these points.

Animals↗