July 1996
WASHINGTON, D.C. Primary infection with human herpesvirus 7 (HHV-7) may cause a highly febrile illness in childhood that may often be complicated by seizures. Little is known about the pathogen, which is relatively new, and it is unclear whether HHV-7 always causes symptomatic disease, according to Mary Caserta, MD.
Although HHV-7 is genetically different from human herpesvirus 6 (HHV-6), clinically the differences are not yet apparent. HHV-7 was first recovered from the CD4+ lymphocytes of a healthy adult in 1990, when cultured under conditions leading to T-cell activation. More isolates have been recovered by similar methods from peripheral blood mononuclear cells (PBMCs) and saliva of healthy and ill children and adults. Large serologic studies have shown widespread human infection with HHV-7, occurring as a primary infection in childhood somewhat later than HHV-6, according to Caserta.
Currently, there is no method to routinely diagnose HHV-7 and there is no specific treatment for infection. Much of what is known or suspected about the virus is based on studies of small numbers of patients that indicate that there is a range of symptoms due to HHV-7 infection, Caserta said in a study presented at the Pediatric Academic Societies' annual meeting here.
As with all human herpesviruses, HHV-7 lies dormant in the host and may reactivate later in life. "If reactivation of the virus in the central nervous system is a cause of recurrent seizures, then this information might provide an other avenue of treatment," Caserta said. Exactly how HHV-7 may manifest itself after the primary infection is unknown.
In a recent study of 560 U.S. children led by Caserta and co-authored by Caroline B. Hall, MD, of the University of Rochester School of Medicine, HHV-7 infection was identified in eight children ranging in age from 3 months to 3 years. Patients exhibited fever (mean 39.7° C), with six children (75%) also developing seizures during the acute illness. Investigators identified HHV-7 primary infection by viral isolation and seroconversion. Nested polymerase chain reaction (PCR) for HHV-6 and HHV-7 was also performed.
Because a high percentage of febrile children developed seizures, HHV-7 may be considered an important pathogen, according to Caserta.
"The findings give credibility to the fact that there are multiple viral infections during childhood," Caserta said. However, whether it was the fever or the HHV-7 infection that caused the seizures is "the million dollar question," she said.
Preliminary serologic studies show the appearance of both HHV-6 and HHV-7 antibodies in patients with prior HHV-6 infection. One patient in the study with positive HHV-6 serology showed a fourfold rise in HHV-6 titer in the absence of detectable viral DNA, suggesting that antibodies to both viruses may cross-react. "It is not going to be easy to diagnose HHV-7 by serology. Serologic methods are probably not going to be 100% reliable," Caserta said. It is not known if there is cross-protection from the antibodies.
Caserta also suggested that HHV-7 may lead to the reactivation of HHV-6 in vivo, or HHV-7 may simply be coincidental with reinfection with HHV-6.
HHV-7 has been linked in a small number of isolated cases to roseola, hepatitis, upper respiratory infection and other febrile illnesses. But because these reports rely on serologic evidence, "they may not accurately reflect the clinical syndrome caused by primary HHV-7 infection," she said.
Caserta stressed that although their study was too small to assess the magnitude of morbidity of HHV-7, the data may serve as a springboard for larger studies.
For more information, see:
- Caserta M, Hall C, Schnabel K, et al. Human herpesvirus-7 (HHV-7) infection in U. S. children. Abstract 996. Presented at the Pediatric Academic Societies' 1996 annual meeting, May 6-10, Washington, D.C.
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