Diagnosis of Human Herpesvirus 6 Infections
D. Diagnosis
Virus isolation is not practicable as a routine diagnostic
procedure. If it is to be attempted, the patient's peripheral
blood mononuclear cells are cultured are the presence of PHA
stimulant for 3-6 days. They are then co-cultivated with
similarly stimulated cord blood lymphocytes. Serology is
generally used to make a diagnosis in a routine laboratory. Both
IgM and IgG can be demonstrated by immunofluorescence. One
problem is that HHV-6 reactivates frequently causing a rise in
both serum IgM and IgG. This has been shown to happen with
concomitant primary EBV infections and during primary or
reactivating CMV infections. It is thought that the serological
response to HHV-6 in these instances is due to reactivation of
latent virus as the result of an infection with another agent
rather than indicating antibody cross-reactivity.
E. Management
Cases of roseala infantum are sporadic and outbreaks have not been described in families or paediatric wards. Most cases of roseala are relatively mild and do not require hospitalization. It is probably very difficult and probably inadvisable to avoid infection.
Other Herpesviruses
1. HHV-7
HHV-7 was first isolated in 1989 from the peripheral blood
lymphocytes of a healthy individual. Since then, HHV-7 has been
isolated from the saliva of as many as 75% of healthy adults.
Antibodies to HHV-7 can be detected in the serum specimens from
90% of the normal population. HHV-7 has yet to be conclusively
with any disease. There is data to suggest that it is able to
cause roseala infantum.
2. Human Herpes Virus 8 (HHV-8)
Through the use of a new molecular biology technique known as representational differential analysis (RDA), whereby the genetic material present in a suspected infected cell is compared to that of an un-infected cell of the same type, herpesvirus-like DNA sequences were discovered in the majority of Kaposi’s sarcoma. This new herpesvirus has now been named HHV-8. There is cumulating evidence for a role of this virus in Kaposi's sarcoma. Since its discovery by in 1994, HHV-8 has been identified in virtually all AIDS- and non-AIDS-related KS lesions. At the same time, several research teams have identified the virus in a subset of other less-uncommon pathologic conditions, including primary effusion lymphomas and multicentric Castleman’s disease. But while a definitive link exists between HHV-8 and these specific malignancies, the precise role that it plays in their development is not completely understood. The pathogenesis of KS is, in fact, a multifactorial process. Some of the factors known to play a role in its development, aside from HHV-8, include altered expression and response to cytokines and angiogenesis. Whether these factors result from or are independent of viral infection is unresolved at this time. Nevertheless, therapeutic strategies have targeted these factors and are now entering clinical trials.
Kaposi's Sarcoma affecting the forearm
Serologic assays for KSHV/ HHV-8 antibodies are now available to test for the presence of the virus. The assays depend on cell lines derived from body cavity-based primary effusion lymphomas, which are infected with up to 100 copies of the virus and are a rich source of a viral latency-associated nuclear antigen (LANA). Studies using LANA assays have found that close to 100% of sera from non-AIDS KS patients are positive for HHV-8 antibodies. In AIDS-related KS, there is a lower (~80%) LANA positivity rate as measured by existing seroassays, probably due to decreased antibody production in patients with late-stage HIV disease.
The rates of HHV-8 infection in the general population of
Mediterranean countries (Italy, Greece, Israel, Saudi Arabia),
where classic KS is seen with relatively high frequency, are
higher than in North America and Northern Europe. Adult
populations in some portions of Africa, where KS has long been
quite common also, have very high infection rates (>50%).
Additional studies have found a strong link between HHV-8
antibody seropositivity and the risk of developing KS. In
HIV-negative blood donors, anti-LANA seropositivity rates are 1%
to 2%, whereas about 30% of HIV-positive gay men have been found
to be seropositive. Moreover, the concordance of positive LANA
serologies with KS prevalence implies that clinically healthy
HIV-positive men who are HHV-8-positive have a high risk of
progression to KS once immunodeficiency supervenes. The HHV-8
seropositivity rate among HIV-positive hemophiliacs or
transfusion recipients, on the other hand, has been reported to
be only 2% to 3%. Similarly, only 3% to 4% of HIV-positive
heterosexual women are KSHV/HHV-8-positive. Indeed HHV-8 is
unique among human herpesviruses in that it is not ubiquitous in
distribution.It is not known why KS predominates in males. It is
possible that hormones play an important role in this regard.
3. Herpes B Simiae
Herpes B Simiae causes disease in old world monkeys similar to that of HSV in humans. In rare instances, it may be transmitted to humans, usually through a monkey bite, where it may cause a severe fatal disease with encephalitis. There had only been 22 reported cases in the literature, of which one case resulted from person-to-person transmission. IV acyclovir and/or ganciclovir had been used in the treatment of suspected cases but their exact value has yet to be determined. The control of infection depends of good procedures in animal houses, where possible, the Herpes B status of the monkeys should be determined and only those which are known to be free of the virus should be used.
