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At least 127 records · Page 7Linked to original sources
PubMed1993

Viral pathogenesis and opportunistic infections.

Knowledge about the pathogenesis and management of HIV infection has increased dramatically over the last decades. Because of advances in drugs, diagnosis and management, HIV-infected patients are living longer. This paper provides current concepts of HIV pathogenesis and antiviral therapy, and an overview of AIDS-related opportunistic infections.

AIDS-Related Opportunistic Infections↗
PubMed1994

A molecular genetic approach to the study of Venezuelan equine encephalitis virus pathogenesis.

Viral pathogenesis can be described as a series of steps, analogous to a biochemical pathway, whose endpoint is disease of the infected host. Distinct viral functions may be critical at each required step. Our genetic approach is to use Venezuelan equine encephalitis virus (VEE) mutants blocked at different steps to delineate the process of pathogenesis. A full-length cDNA clone of a virulent strain of VEE was used as a template for in vitro mutagenesis to produce attenuated single-site mutants. The spread of molecularly cloned parent or mutant viruses in the mouse was monitored by infectivity, immunocytochemistry, in situ hybridization and histopathology. Virulent VEE spread through the lymphatic system, produced viremia and replicated in several visceral organs. As virus was being cleared from these sites, it began to appear in the brain, frequently beginning in the olfactory tracts. A single-site mutant in the E2 glycoprotein appeared to block pathogenesis at a very early step, and required a reversion mutation to spread beyond the site of inoculation. The feasibility of combining attenuating mutations to produce a stable VEE vaccine strain has been demonstrated using three E2 mutations.

Amino Acid Sequence↗
PubMed2006

The cysteine-histidine-rich region of the movement protein of Cucumber mosaic virus contributes to plasmodesmal targeting, zinc binding and pathogenesis.

Viral movement proteins (MPs) are central to the establishment of viral pathogenesis, and yet relatively little is understood about the structural and functional aspects of MPs or about the host factors on which they depend. Through chemical mutagenesis of transgenic Arabidopsis expressing Cucumber mosaic virus (CMV) MP fused with the green fluorescent protein, we have studied the function of a central region of the MP, defined by a number of conserved cysteine and histidine residues (Cys-His-rich region), which potentially functions as a zinc-binding domain. Transient expression of mutant MPs identified through an in planta screen for altered MP function or constructed with altered putative zinc ligands through site-directed mutagenesis showed that mutations in the Cys-His-rich region affected localization to and trafficking through plasmodesmata. In vitro zinc-binding analysis revealed that wild type (wt) CMV MP had the ability to bind zinc and that movement-defective mutants bound zinc with less affinity than wt MP. Furthermore, a correlation between the association of the MP with plasmodesmata and virus pathogenesis was shown. We discuss roles of the Cys-His region in biochemical and biological functions of the MP during virus movement.

Amino Acid Sequence↗
PubMedDate not supplied

Pathogenesis of viral infections: the role of the immune response.

The replication and spread of viral infections in the human host occurs by a variety of mechanisms. Replication of genetic sequences varies with the initial starting material (DNA or RNA). Proliferation in the host may be by direct cell-to-cell spread, cell lysis, or budding from the infected cell's membrane. Various viremic or localized stages have been demonstrated. Particular tropisms are thought to be due to the presence of particular receptors. Recent advances in molecular biology, which will be reviewed, have expanded our capacity to detect the genetic footprints of viruses, and our understanding of viral pathogenesis. The host immune system must be prepared for an array of mechanisms to prevent or ameliorate virus infection. These may take the form of specific and nonspecific antibody formation, or the generation of specific cytotoxic lymphocytes that are restricted by the HLA system. In addition, nonspecific mediators, such as the complement system, interferon, and other lymphokines, play a significant role in the pathogenesis of viral infections. While the greatest portion of these cellular efforts are aimed at the destruction or elimination of viral infection, the immune response may augment the pathogenic effect under some circumstances. The formation of immune complexes may also contribute to the pathogenesis of some infections.

Antibody Formation↗
PubMed1987

Molecular and genetic aspects of the pathogenesis of viral infections of the central nervous system.

Viral pathogenesis can be defined in terms of a series of successive interactions between a virus and its target host. In order for a virus to injure a target organ such as the central nervous system (CNS), it must first enter the host animal, replicate in some primary site near its place of entry, spread from this site to the CNS and infect and injure specific populations of cells within the CNS. At each of these steps, the virus must avoid or overcome a variety of immunological and nonimmunological host defenses. It has recently become possible to begin to identify the role of specific viral genes and the proteins they encode at specific steps in the pathogenesis cycle. This review focuses on current knowledge concerning the molecular and genetic basis for the pathogenesis of viral infections of the CNS. Emphasis is placed on recent research with a wide variety of neurotropic viruses including reoviruses, bunyaviruses, lymphocytic choriomeningitis virus, rabies virus, polio virus, herpes viruses, lentiviruses, and the unconventional agents responsible for disease such as scrapie.

Humans↗
PubMed1995

The role of transgenic knockout models in defining the pathogenesis of viral heart disease.

The pathogenesis of viral myocarditis involves contributions from the virus, the immune system and myocytes. In defining the molecular contributions in the disease process, modulations of the components of the immune system through transgenic knockout models provide useful insights. Advantages of the transgenic knockout models are that they allow biological evaluation of the importance of a particular molecule in the physiological context of an intact organism. Furthermore, the techniques of transgenic knockout models are now standardized, even though they are still technically challenging and time consuming. An example in myocarditis is the IRF-1 knockout mouse, where there is a complete absence of the inducible form of nitric oxide synthetase in the tissues. These animals are exquisitely sensitive to coxsackieviral infection, with extremely high mortality. On the other hand, CD4 knockouts appear to still have myocarditis in an autoimmune myocarditis model, while p56lck knockouts (the T-cell tyrosine kinase signalling molecule) appears to be free of viral myocarditis. These elegant systems of molecular manipu-lation should allow us unique insights into the pathogenesis of myocarditis.

Animals↗
PubMed2004

Technical knockout: understanding poxvirus pathogenesis by selectively deleting viral immunomodulatory genes.

The study of viral pathogens with genomes as large and complex as poxviruses represents a constant experimental challenge. Advances in recombinant DNA technologies have provided sophisticated methods to produce mutants defective in one or more viral genes, termed knockout (KO) viruses, thereby facilitating research into the impact of specific gene products on viral pathogenesis. Such strategies have rapidly advanced the systematic mining of many poxvirus genomes and enabled researchers to identify and characterize poxvirus genes whose functions represent the culmination of host and pathogen coevolution. Of particular interest are the multiple classes of virus-encoded immunomodulatory proteins that have evolved specifically to allow poxviruses to evade, obstruct or subvert critical elements within the host innate and acquired immune responses. Functional characterization of these viral genes by generating KO viruses and investigating the phenotypic changes that result is an important tool for understanding the molecular mechanisms underlying poxvirus replication and pathogenesis. Moreover, the insights gained have led to new developments in basic and clinical virology, provided a basis for the design of new vaccines and antivirals, and increased the potential application of poxviruses as investigative tools and sources of biotherapeutics for the treatment of human diseases.

Adjuvants, Immunologic↗
PubMed2000

Dengue viral infections; pathogenesis and epidemiology.

Dengue viral infections affect up to 100 million individuals per year. Dengue haemorrhagic fever is a clinical form of disease characterised by intravascular fluid loss. There has been a marked increase in the incidence of this form of the disease over the last few decades, associated with significant mortality, particularly in the paediatric population. A number of theories relating to the pathogenesis of dengue haemorrhagic fever exist that have evolved from the analysis of the epidemiology of this disease. Virological and immunopathological factors are both important but the exact mechanisms for the disease are unknown.

Africa↗
PubMed1992

The Zvonimir Dinter Memorial Lecture. New insights into the pathogenesis of viral infection.

Interesting recent highlights into the pathogenesis of viral infections have come from: (1) Studies of viruses that persist in cells and modify cell function without causing cell damage. (2) Transgenic mouse studies showing how tissue-specific transcriptional activators control virus expression and can determine viral tropism. (3) Studies of the influence of cell differentiation on viral expression. (4) The exploding world of cytokines, whose baffling complexity and multiple interactions are subjects of intense study. (5) Studies of the interaction of viruses with the immune system. In each case, no molecular studies are giving unprecedented insights into disease processes. However, even when viral genomes are sequenced and virulence genes identified there are additional daunting steps before we understand the role of a given gene product in pathogenesis.

Animals↗
PubMed1997

HIV-1 Vpr suppresses immune activation and apoptosis through regulation of nuclear factor kappa B.

The HIV-1 accessory gene product Vpr can influence viral pathogenesis by affecting viral replication as well as host cell transcription and proliferation. We have investigated the effects of Vpr on host cell activation and confirm that it influences cellular proliferation. However, we have also found that Vpr modulates T-cell receptor (TCR)-triggered apoptosis in a manner similar to that of glucocorticoids. In the absence of TCR-mediated activation, Vpr induces apoptosis whereas in its presence, Vpr interrupts the expected induction of apoptosis. This regulation of apoptosis is linked to Vpr suppression of NF-kappa B activity via the induction of I kappa B, an inhibitor of NF-kappa B. Further, Vpr suppresses expression of IL-2, IL-10, IL-12, TNF alpha and IL-4, all of which are NF-kappa B-dependent. The effects of Vpr could be reversed by RU486. Our finding that Vpr can regulate NF-kappa B supports the hypothesis that some aspects of viral pathogenesis are the consequence of cell dysregulation by Vpr.

Animals↗
PubMed1980

The pathogenesis of viral leukoencephalomyelitis-arthritis of goats. I. Persistent viral infection with progressive pathologic changes.

The pathogenesis of viral leukoencephalomyelitis of goats was studied in newborn and adult goats using purified, concentrated leukoencephalitis virus. The disease could be transmitted using purified leukoencephalitis virus or tissue suspensions from a goat experimentally infected with leukoencephalitis virus. As early as 1 week following inoculation, goats developed lesions in the brain, joint, and lung. Lesions persisted 8 to 21 months, were not age-dependent, and were inflammatory in character. In the brain they were accompanied by demyelination. Virus could be isolated from experimental goats by cocultivation of peripheral blood leukocytes and by explantation of tissues beginning a week after inoculation and throughout the life of the goat. These studies confirm that leukoencephalitis virus is the etiologic agent of leukoencephalitis-arthritis of goats and produces a persistent infection characterized by demyelinating encephalitis, progressive arthritis, and interstitial pneumonia.

Age Factors↗
PubMed1992

Immune mechanisms in the pathogenesis of viral diseases: a review.

Three immunopathological mechanisms may determine the pathogenesis of viral diseases in animals. (1) A variety of viruses causes transient or prolonged immunosuppression by infecting lymphoreticular tissues and interacting with components of the immune system. (2) In persistent viral infections effective immune responses may result in tissue damage. The mechanisms involved are T-cell-mediated destruction of infected cells and delayed-type hypersensitivity. (3) In a number of viral diseases pathogenic immune complexes are formed when antibodies are produced and react with viral antigen molecules persisting in the host. The selected examples of immune dysfunction are the focus of this review.

Animals↗
PubMed2004

Retroviral spread by induction of virological synapses.

Cells of the immune system communicate via the formation of receptor-containing adhesive junctions termed immunological synapses. Recently, retroviruses have been shown to subvert this process in order to pass directly from infected to uninfected immune cells. Such cell-cell viral dissemination appears to function by triggering existing cellular pathways involved in antigen presentation and T-cell communication. This mode of viral spread has important consequences for both the virus and the host cells in terms of viral pathogenesis and viral resistance to immune and therapeutic intervention. This review summarises the current knowledge concerning virological synapses induced by retroviruses.

HIV Infections↗