Review of 3200 serially received CSF samples submitted for type-specific HSV detection by PCR in the reference laboratory setting

Predominant type 1 CMV-Specific memory T-helper response in humans: evidence for gender differences in cytokine secretion

“…This has been observed in parasitic (reviewed in [40]) and viral infections. For example, the incidence and seroconversion of HSV-1 or HSV-2 [41][42][43] and human papilloma virus [44 -46] is higher among women. Before initiation of antiretroviral therapy, survival of HIV-infected women was shorter than in men [5,6], whereas seroconversion and disease progression in HIV-infected women is observed at lower viral load than in men [7][8][9][10][11][12].…”

HSV, Axonal Transport and Alzheimer‘s Disease: in Vitro and in Vivo Evidence for Causal Relationships

“…The prevalence of HSV-1 can be determined by testing serum for antibodies to HSV-1 [8,9], by the detection of HSV-1 DNA in cerebrospinal fluid (CSF) [10], or in TG acquired at autopsy [11]. Such studies have revealed endemic infection rates of 31% in children aged 6–14, rising to 49% in adults aged 14–49, and to a high of 80–90% in the population over 65.…”

“…Detection of viral DNA in the CSF demonstrates that, even during clinically silent infections, virus replicates in the CNS [10]. Although sensory innervation of the meninges emanates from the TG and superior cervical ganglia, these sensory nerve endings occur in the outer meningeal surface with little direct access to the CSF.…”

HSV-1 and Alzheimer’s disease: more than a hypothesis

“…Many infectious agents whose pathogenetic role has been established in other CNS diseases (e.g., varicella zoster virus, causing meningitis or encephalitis; Epstein–Barr virus, associated to both multiple sclerosis and CNS lymphoma; human herpes virus 6, associated to seizure in children) may infect subjects without producing evident clinical signs. On the other hand, even in the presence of “clinically silent” infection, virus may periodically reactivate and replicate in the CNS (Peter and Sevall, 2001; Bearer, 2012). There is no clear evidence on whether HSV-1 reaching the brain and infecting neurons resides there in latent form.…”

“…There is no clear evidence on whether HSV-1 reaching the brain and infecting neurons resides there in latent form. However, the detection of HSV-1 DNA in the cerebro-spinal fluid (Deatly et al, 1988; Peter and Sevall, 2001; Plentz et al, 2008) suggests that HSV-1 replicates in the CNS (Bearer, 2012). The presence of HSV-1 proteins in hippocampal neurons of mice infected intraperitoneally with HSV-1 was demonstrated by Burgos et al (2006a) who also showed that virus is reactivated by hyperthermia.…”