Evidence of human herpesvirus 6 in Sjögren syndrome and sarcoidosis.
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Base Sequence↗
Biomedical subjects
A M Fillet
Publications and source records attributed to A M Fillet.
Difference in permissiveness of human fibroblast cells to variants A and B of human herpesvirus-6.
Human herpesvirus-6 (HHV6) is a lymphotropic virus genetically related to human cytomegalovirus (CMV) and for which two variants, A and B, have been distinguished. Human CMV is usually cultivated with human fibroblasts (HF). The lack of cell lines useful for HHV6 isolation and propagation led us to investigate whether HHV6 variants A and B could infect HFs as CMV does. Isolates of HHV6 variants A and B were used to infect MRC-5 HFs. HHV6 infection was detected by means of immunoperoxidase assay using three specific monoclonal antibodies. HHV6-specific antigens were detected in 88 and 38% of cases after infection with variants A and B, respectively. The highest number of HHV6-antigen-positive cells was obtained at 4-5 days p.i. The titre of HHV6 stocks was determined in parallel by immunoperoxidase assay on HFs and by observation of cytopathic effect using serial dilutions on peripheral blood mononuclear cells (PBMC). The number of infectious particles inducing the appearance of antigen-positive HF cells was consistently lower than the titre of virus stocks, expressed as TCID50. The amount of HF-associated HHV6 DNA was measured using limiting dilution PCR assay; it was significantly increased during 4-day infection in the case of variant A but not variant B. The yield of virus from infected HFs was demonstrated only for variant A by the serial propagation of virus from HFs to PBMCs and by the increase in cell-free HHV6 DNA in HF culture supernatant. Our results show that HHV6 can reproducibly infect HFs, albeit at a low level, and that HFs are more permissive to variant A than to variant B, as reported previously for PBMCs and human T-cell lines.
Antigens, Viral↗
[Efficacy of cidofovir in an HIV infected patient with an acyclovir and foscarnet resistant herpes simplex virus infection].
BACKGROUND: We report the case of an AIDS patient, whose persistant HSV2 ulceration was clinically and phenotypically resistant to acyclovir and foscarnet. Only five clinical isolates of simultaneous acyclovir and foscarnet resistance have been previously described. CASE REPORT: This patient, without history of opportunistic infection, was hospitalized for a recurrent scrotal ulceration resistant to several antiviral treatment such as acyclovir, valacyclovir or foscarnet. The CD4 count was stable at 150/mm(3) and the HIV viral load was below detection level. The last recurrence appeared rapidly under valacyclovir therapy which had been introduced after 65 days of foscarnet therapy. Thus, the patient received a new dose of foscarnet. After initial efficacy, the ulceration increased once again. HSV2 phenotypic determination was done and detected, at that time, a double resistance to acyclovir and foscarnet. Healing was obtained with intravenous cidofovir. DISCUSSION: Foscarnet and acyclovir resistance in an HSV2 isolate is rare. This report presents several particularities. First, whereas the earlier published patients with an acyclovir and foscarnet resistant strain were widely immunocompromised, this was not the case for our patient. Secondly, in contrast with most precedent observations in which acyclovir-resistant strain disappeared after foscarnet therapy, in our case the acyclovir resistant strain remained after foscarnet therapy. Finally, few reports concerned the clinical efficacy of cidofovir in HSV infection. In this case, we proved that intravenously cidofovir was highly and rapidly effective on acyclovir and foscarnet resistant strains.
AIDS-Related Opportunistic Infections↗
[The discovery of three novel human viruses, human herpesviruses 6, 7, and 8].
Three novel human herpesviruses have been discovered in the last years: human herpesvirus 6 (HHV-6) in 1986, human herpesvirus 7 (HHV-7) in 1990, human herpesvirus 8 (HHV-8) in 1994. HHV-6 and HHV-7 were identified after their isolation from blood lymphocyte cultures, while HHV-8 was first detected by means of a specific molecular biology approach in the search for the etiologic agent of Kaposi's sarcoma. The three viruses infect lymphocytes, T-cells in the case of HHV-6 and HHV-7, B-cells in the case of HHV-8. Human infection with HHV-6 and HHV-7 is ubiquitous and widespread while HHV-8 infection seems to be more restricted, at least in Western countries. The propagation in cell culture in vitro can be done easily with HHV-6, with more difficulties in the case of HHV-7 and has not been completely obtained in the case of HHV-8. The polymerase chain reaction is the common method for the detection of these three viruses in human samples. The oncogenic role of HHV-6 and HHV-7 which were both classified in Betaherpesvirinae subfamily has not been convincingly demonstrated. HHV-8, classified as a member of Gammaherpesvirinae subfamily, is strongly associated with three lymphoproliferative diseases: Kaposi's sarcoma, Castleman's disease and primary effusion lymphomas.
Herpesviridae Infections↗