Human herpesvirus 7
Human herpesvirus 7 (HHV-7) is one of eight known members of the Herpesviridae family. It acts together with HHV-6 to cause the childhood illness, Roseola. HHV-7 resides mostly in the immune cell named CD4+ T (also known as CD4 cells, T-helper cells or T4 cells) and causes the downregulation of CD4 transcription (in simpler terms, causes the decreased production of a protein on the cell membrane used to signal to other immune cells). CD4 T cells from ME/CFS patients produced less interferon-gamma than did cells from controls, but whether this is related to HHV-7 has not been determined.
HHV-7 in ME/CFS[edit | edit source]
- 2000, a study done by the CDC in Atlanta, Georgia concluded: "Primary infection with HHV-6 or HHV-7 is not likely to be causally associated with CFS, because [the] infection is virtually ubiquitous by the age of 2–5 years. Moreover, it is unlikely that reactivation of latent HHV-6 or HHV-7 is causally associated with a substantial proportion of cases of CFS because of the lack of consensus among studies and because reactivation of most latent herpesviruses is common, occurs sporadically, and is usually asymptomatic."
- 2006, a study at Riga Stradins University, Latvia, was done on 17 CFS patients, 12 patients with unexplained chronic fatigue and 20 blood donors: They found no difference in the prevalence of latent/persistent single viral infections between the different groups, but dual infection rate was significantly higher in CFS patients. Active HHV-6 and dual (HHV-6 + HHV-7) infections were detected in the CFS patient group only and the frequency of HHV-7 reactivation was also significantly higher in these patients. The researchers conclusion was: "HHV-6 and HHV-7 may be involved in the pathogenesis of CFS and reactivation of both viruses may provoke changes in the phenotype of circulating lymphocytes."
- 2012, a study at Riga Stradins University, Latvia, done on 108 CFS patients and 90 controls concluded: "The association between occurrence of ME/CFS clinical symptoms, HHV-6, HHV-7 and B19 infection/coinfection reactivation and increased expression levels of TNF-α and IL-6 allows suggesting that these immunomodulating pathogens are involved in ME/CFS etiopathogenesis. Their role as trigger factors could not be excluded. The correlation of distinctive active viral infection with various types of clinical symptoms shows necessity of simultaneous study of these viral infections for identification of possible subsets of ME/CFS."
Notable studies[edit | edit source]
- 2016, Human herpesvirus 6 and 7 are biomarkers for fatigue, which distinguish between physiological fatigue and pathological fatigue
Learn more[edit | edit source]
- 2018, A Common Virus May Play Role in Alzheimer’s Disease, Study Finds by Pam Belluck via NY Times
See also[edit | edit source]
References[edit | edit source]
- Visser, J; Blauw, B; Hinloopen, B; Brommer, E; de Kloet, ER; Kluft, C; Nagelkerken, L (1998), "CD4 T lymphocytes from patients with chronic fatigue syndrome have decreased interferon-gamma production and increased sensitivity to dexamethasone.", Journal of Infectious Disease, 177 (2): 451-4, PMID 9466535
- Chapenko, S.; Krumina, A.; Kozireva, S.; Nora, Z.; Sultanova, A.; Viksna, L.; Murovska, M. (2006), "Activation of human herpesviruses 6 and 7 in patients with chronic fatigue syndrome.", Journal of Clinical Virology, Supplement 37 (Suppl 1): S47-51, doi:10.1016/S1386-6532(06)70011-7, PMID 17276369
- Chapenko, S.; Krumina, A.; Logina, I.; Rasa, S.; Chistjakovs, M.; Sultanova, A.; Viksna, L.; Murovska, M. (2012), "Association of active human herpesvirus-6, -7 and parvovirus B19 infection with clinical outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome.", Advances in Virology, doi:10.1155/2012/2050850
- Aoki, R; Kobayashi, N; Suzuki, G; Kuratsune, H; Shimada, K; Oka, N; Takahashi, M; Yamadera, W; Iwashita, M; Tokuno, S; Nibuya, M; Tanichi, M; Mukai, Y; Mitani, K; Kondo, K; Ito, H; Nakayama, K (2016), "Human herpesvirus 6 and 7 are biomarkers for fatigue, which distinguish between physiological fatigue and pathological fatigue", Biochemical and Biophysical Research Communications, 478 (1): 424-30, doi:10.1016/j.bbrc.2016.07.010, PMID 27396623