It was previously thought that primary infection of HHV-6 in infants and young children lead to roseola and febrile illnesses. This infection was attributed to HHV-6B (Yamanishi et al., 1988). Some of the symptoms identified include diarrhea, vomiting, seizure, nasal congestion, rash and high fever. Similar symptoms were noted in Africa in children and the DNA analysis from the peripheral blood from these children revealed HHV-6A infections (Hidaka et al., 1997; Kasolo et al., 1997; Randhawa et al., 1997). It is, therefore, obvious that both variants A and B participate in infecting growing children with identical pathologies. Hall et al. (1994) also observed that one third of congenital infection was due to HHV-6A. Later on these children still retained HHV-6A DNA. There have not been longitudinal follow-up studies to assess whether these children with congenital HHV-6A infection could be at risk of developing a central nervous system (CNS) illness such as multiple sclerosis.
One complication of CNS disease with HHV-6 could be seizures. CNS involvement may lead to meningitis and encephalitis or encephalopathy (Suga et al., 1993). The CNS is most likely one of the sites of persistence of virus following primary infection. Both variants have been detected in the cerebral spinal fluids (CSF). There is more recent evidence that HHV-6A may have a greater neurotropism (Aberle et al., 1996; Hall et al., 1998). In this study 84 of 660 CSF samples from children under 3 years of age with or without febrile illness were HHV-6 positive by PCR. Seven children had primary infection, and in the remaining 77, HHV-6 was detected in periferal blood mononuclear cells (PBMC) and CSF in 30 (39%). In CSF alone, 47 (61%) HHV-6A was detected more frequently than in PBMCs. In children who had HHV-6 in PBMCs and CSF, variant B was detected in the former and HHV-6A in the latter. There is considerable evidence showing that severe meningitis was caused by HHV-6B in an immune-competent woman who was treated with ganciclovir (Birnbaum et al., 2005). Cases of encephalitis have been reported frequently with HHV-6 infection as a result of complications. In some cases, variant A has been detected and in other cases variant B has been reported (Clark, 2000; DeBolle et al., 2005). In the early studies as well as in some more recent studies, attempts have been made to identify the variant (Isaacson et al., 2005). Whitley et al. (2005) believes that rare cases of HHV-6 infections of the CNS exist. At the present time only PCR (Taqman) assay is utilized that may not be sensitive enough, because if the HHV-6 persists in low DNA copy numbers the assay may not detect it. New, more sensitive serological assays are needed to detect active infection in patients with low-grade infection.
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