Persistent reactivable latent herpes simplex virus infection in trigeminal ganglia of mice treated with antiviral drugs

Persistent reactivable latent herpes simplex virus infection in trigeminal ganglia of mice treated with antiviral drugs

Wildy, P., Field, H. The same may also hold for ganglia and vagina after genital infections. This presents a major impediment to the use of HSV as a vector system. While significant amounts of interferon were produced by C 1300 cells when challenged with Newcastle Disease Virus (NDV) or when treated with poly I:C, HSV-induced interferon could not be detected in either the acutely or persistently infected cell lines. The TCRBV genes utilized by these clonotypes were sequenced, and clonotype-specific probes were used to longitudinally track these clonotypes in PBMC and genital lesions. Treatment of infections due to herpesvirus in humans: A critical review of the state of the art, 101–108. Survivor cells continued to express HSV-1-specific antigens, however, as detected by indirect immunofluorescence and by surface iodination followed by immunoprecipitation and polyacrylamide gel electrophoresis.

Measurement of serum Abs to HSV-1 at different times revealed that anti-HSV-1 Ab concentrations approached a plateau in mice by 30 days PI but remained at high levels 67 and 125 days PI. J., Bell, S. pylori infection, use of NSAIDs, alcohol, or smoking were not associated with chronic erosions. B., Nash, A. Get a printable copy (PDF file) of the complete article (1.5M), or click on a page image below to browse page by page. Antimicrob. Agents Chemother.15, 554–561 (1979).

Silent spread is the rule for HSV-2, not the exception. R. During both productive and latent infections, the genome assumes a configuration indicative of end-joining, because genomic joint sequences increase in abundance relative to their homologous counterparts at the genomic termini (12–15). R.: The activity of iododeoxyuridine, adenine arabinoside, cytosine arabinoside, ribavirin and phosphonoacetic acid again herpes virus in hairless mouse model. J. Antimicrob. Chemother.3A, 91–98 (1977).

Helgestrand, E., Alenius, S., Johansson, N. E. Current Chemotherapy and Infectious Disease Preceedings of the 11th. It may also act by modulating the activities of ICP4 and ICP0 (75, 104), as well as the modification state of ICP4 (75, 92, 112). Kern, E. HSV-1 strain E115 and HSV-2 strain 333 were used throughout unless otherwise noted. A., Overall, J.

Persistent reactivable latent herpes simplex virus infection in trigeminal ganglia of mice treated with antiviral drugs
C. jr., Reno, J. M., Boezi, J. A.: Treatment of experimental herpesvirus infections with phosphonoformate and some comparisons with phosponoacetate Antimicrob. Agents Chemother.14, 817 to 823 (1978). Klein, R. J., Friedman-Kien, A.

E.: Latent herpes simplex virus infections in sensory ganglia of mice after topical treatment with adenine arabinoside and adenine arabinoside monophosphate. Antimicrob. Agents Chemother.12, 577 to 581 (1977). AdS.11E4(ICP0), an adenovirus vector that expresses ICP0, and AdS.11D, the empty adenoviral vector, were provided by Douglas Brough (GenVec, Gaithersburg, MD) and have been described (18). J., Friedman-Kien, A. E., Fondak, A. A., Buimovici-Klein, E.: Immune response and latent infection after topical treatment of herpes simplex virus infection in hairless mice.

Infect. Immun.16, 842–848 (1977). Elion, G. J., Friedman-Kien, A. In support of this hypothesis, elimination of VP16, ICP4, and ICP0 activity reduced cytotoxicity but also reduced gene expression (88, 89). B.: Orofacial herpes simplex virus infection in hairless mice: Latent virus in trigeminal ganglia after topical antiviral treatment. 1 at the time of the lesion from which these clones were originally isolated (February 1995), 1 mo (March 1995), 6 mo (August 1995), and 2 years (February 1997) post-lesion onset and from CD8+ PBMC from an unrelated HSV-seropositive individual (ctrl CD8+).

Immun.20, 130–135 (1978). Klein, R. J., de Stefano, E., Brady, E., Friedman-Kien, A. E.: Latent infections of sensory ganglia as influenced by phosphonoformate treatment of herpes simplex virus-induced skin infections in hairless mice. Antimicrob. Agents Chemother.16, 266–270 (1979). Kristensson, K., Svennerholm, B., Persson, L., Vahlne, A., Lycke, E.: Latent herpes simplex virus trigeminal ganglionic infection in mice and demyelination in the central nervous system.

J. Neurol. Sciences43, 253–264 (1979). Subak-Sharpe, J. The eluted DNA was digested with both BamHI and SacI (New England Biolabs) according to the manufacturer’s instructions. R.: In:Burke, D. C., Rusell, W.

C. (eds.), Control processes in virus multiplication. Viral information controlling DNA and RNA animal virus replication, 363–403. A., Inglis, M.

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