Human herpesvirus 6: General data and infections in organ transplantation and hematopoietic stem cell grafts

Citation
J. Fontan et al., Human herpesvirus 6: General data and infections in organ transplantation and hematopoietic stem cell grafts, PRESSE MED, 28(3), 1999, pp. 149-156
Citations number
60
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
PRESSE MEDICALE
ISSN journal
07554982 → ACNP
Volume
28
Issue
3
Year of publication
1999
Pages
149 - 156
Database
ISI
SICI code
0755-4982(19990123)28:3<149:HH6GDA>2.0.ZU;2-S
Abstract
General data: Human herpesvirus 6 (HHV-6) infects 90% of the human populati on before the age of 4 years, recognized as a childhood disease (sixth dise ase) or with no clinical manifestation. HHV-6 DNA has partial homogly with cytomegalovirus DNA. Two variants, A and B, are known. The main target cell s are CD4+ T cells and macrophages via a partially elucidated mechanism. Pr imary infection is followed by a latency period and episodes of reactivatio n. Truly protective targets of the immune response are unknown. Poorly understood natural history: in organ transplant or hematopoietic ste m cell recipients, the natural history of HHV-6 infection is difficult to e stablish because of small sample size in certain series, the lack of contro ls both for patients and samples and differences in the sensitivity of diag nostic tests. Serology is non-specific and cannot be used to study reinfect ion. Different studies have relied on culture and isolation, detection of v iral antigens with monoclonal antibodies and PCR using mononucleated cells, serum and plasma. Pathogenicity: In heart transplant recipients, HHV-6 infection can cause he patitis and pancreatic or upper digestive tract disorders. It has also been suggested that HHV-6 could cause complications in liver transplant recipie nts and be involved in rejection episodes after kidney transplantation. In bone marrow graft recipients, HHV-6 could cause early onset interstitial pn eumopathy, myelosuppression phenomena and aggravated graft versus host reac tions. Nevertheless, viral DNA has been found in certain healthy controls. Other possibilities: HHV-6 could also be a co-factor worsening cytomegalovi rus infections as has been suggested in liver, heart and bone marrow recipi ents. A few cases of HHV-6 encephalitis have been reported in the literatur e and would appear to be authentic in transplanted or grafted subjects. Gan ciclovir is effective. However, the practical clinical impact of HHV-6 infe ction remains to be established.