In memory of Jamie Inglis,
15th January 2013
It is with a heavy heart that I approach this week’s Micrognome blog, knowing that our family has lost one of its own to the childhood cancer, neuroblastoma. The story of Jamie Inglis’ spirited fight with the disease is told elsewhere. It does not have a happy ending. But please take a look and be inspired by what can be achieved when we concentrate our efforts against diseases we can’t control. In his last few weeks Jamie suffered from a human herpes virus 6 infection. Many of the kind folks who funded his hospital treatment will have wondered what this anonymous virus was. In his tragically short life, Jamie’s infectious smile inspired many people to extraordinary acts of generosity. If you have not already done so, make a donation in memory of Jamie to the Neuroblastoma Alliance so that more children with neuroblastoma can receive the emerging therapies that allow them to experience a normal childhood.
This is HHV6, human herpesvirus 6:
Who gets infected? Almost everyone gets infected by HHV6 by the age of 2. Studies show evidence of infection in the general population throughout the first year of live.
What does the virus do? Originally known as human B cell lymphotropic virus, HHV6 is mainly transmitted in saliva and passes via the oropharynx into regional lymphoid tissues, to the body’s mononuclear cells where it avoids immune system detection. It is a DNA virus that burrows into lymphoid cells via a molecule called CD46, then lurks there undetected. The majority of infections are probably asymptomatic. There are a variety of clinical syndromes in those who develop symptoms of infection:
- Fever in infants – one of the commonest causes of paediatric hospital admission for febrile illness
- Febrile convulsion – or very rarely meningitis or encephalitis
- Roseola infantum/sixth disease/ exanthem subitum – fever, upper respiratory symptoms and lymphadenopathy for 3-5 days followed by the characteristic raised, blanching but non-pruritic rash.
- Infectious mononucleosis – the lymphotropic nature of HHV6 make is a potential candidate for an infectious mononucleosis-like syndrome, normally caused by Epstein-Bar virus
- Infections in the immunocompromised – one of the latent viruses that contribute to the waves of viral infection that follow solid organ or stem cell transplant. The role of HHV6 is a little obscure because it is almost universally present and its association with organ damage is confounded by the presence of other viruses at the same time (e.g. HHV7 or CMV). Recent studies indicate a possible active contribution in compromised patients.
How can you detect infection? High prevalence means serological tests have very limited benefit. A rising titre of IgG antibodies is considered evidence of recent infection. HHV6 can be cultured under lab conditions, but PCR assays on serum or plasma are increasingly used to show active infection.
Does it need treatment? In the vast majority of children HHV6 causes a benign infection that requires only supportive care. Some evidence for benefit in immunocompromised patients with active HHV6 infection, but needs to be understood in the context of other viral co-infection. Is it the primary cause of a disease process, or the consequence of other pathophysiology?
How would you treat it? In vitro susceptibility is similar to CMV. Acyclovir is inactive. Ganciclovir has variable activity. Cidofovir and foscarnet appear active in vitro. How this translates to clinical efficacy is difficult to predict.
Geek sheet (MicrobeWiki on HHV6 genome integration)