PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16297742

Viral arthritis.

Leonard H Calabrese·Stanley J Naides
View original source ↗Export metadata ↓

Abstract

The role of viruses in the development of acute and chronic arthritis is complex, because viruses are ubiquitous, and all human beings are occasionally afflicted by viral infections. In general, most viral infections are acute and self-limiting and survive by infecting one susceptible host, then moving on to another. Some viruses establish prolonged latency in the host after acute infection, whereas other agents produce chronic infections following the primary stage. The mechanisms whereby these infections produce arthritis are diverse and still poorly understood, but are clearly influenced by both host and viral factors. This review addresses these and other common forms of viral arthritis, such as that caused by parvovirus B19.

Explore related subjects

Alphavirus InfectionsAntiviral AgentsArthritis, InfectiousHIV InfectionsHTLV-I InfectionsHepatitis BHepatitis CHumansParvoviridae InfectionsRubellaJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Leonard H Calabrese, Stanley J Naides. 2005. Viral arthritis.. https://doi.org/10.1016/j.idc.2005.09.002

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Heparan sulfate binding can contribute to the neurovirulence of neuroadapted and nonneuroadapted Sindbis viruses.

Cell culture-adapted laboratory strains of Sindbis virus (SB) exhibit efficient initial attachment to cell surface heparan sulfate (HS) receptors. In contrast, non-cell-adapted strains, such as the SB consensus sequence virus TR339, interact weakly with HS and cell surfaces. Regardless of their HS binding phenotype, most SB strains do not cause fatal disease in adult mice, whether inoculated subcutaneously (s.c.) or intracranially (i.c.). However, laboratory strains of SB can be rendered neurovirulent for adult mice by introduction of a glutamine (Gln)-to-histidine (His) mutation at position 55 of the E2 envelope glycoprotein. In the current work, we have determined that E2 His 55-containing viruses require a second-site mutation (Glu to Lys) at E2 position 70 that confers efficient HS binding in order to exhibit virulence for adult mice and that virulence is correlated with very high infectivity for many cell types. Furthermore, introduction of E2 Lys 70 or certain other HS-binding mutations alone also increased morbidity and/or mortality over that of TR339 for older mice inoculated i.c. However, all viruses containing single HS-binding mutations were attenuated in s.c. inoculated suckling mice in comparison with TR339. These results suggest that HS binding may attenuate viral disease that is dependent on high-titer viremia; however, efficient cell attachment through HS binding can increase virulence, presumably through enhancing the replication of SB within specific host tissues such as the brain.

Alphavirus Infections↗
PubMed2006

Correlation between breakdown of the blood-brain barrier and disease outcome of viral encephalitis in mice.

Changes in the permeability of the blood-brain barrier (BBB) were evaluated in two mouse models of viral encephalitis. The ability of sodium fluorescein (NaFl) to cross the BBB from the serum into the central nervous system was assayed in animals inoculated with virulent strains of either Banzi or Semliki Forest viruses. To test the hypothesis that increases in BBB permeability were associated with poor disease outcome subsequent experiments measured BBB permeability in conjunction with treatment with the interferon inducer Ampligen (poly I:poly C(12)U). A single intraperitoneal injection of Ampligen (1 mg/kg) administered either 24 h or 4-6 h before, but not 24 h after, virus inoculation with Banzi virus provided significant improvements in survival, viral brain titers, weight change and BBB permeability. In comparison, a similar treatment with Ampligen administered either 24 h or 4-6 h before inoculation with Semliki Forest virus was able to significantly improve weight change, and BBB permeability, but only animals receiving Ampligen 4-6 h pre-virus showed a significantly improved mortality. In general, it was found that evaluation of BBB permeability was a more sensitive indicator of disease outcome and the antiviral efficacy Ampligen than either weight change or brain viral titers.

Alphavirus Infections↗