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Herpes Simplex Virusand the Nervous System P. G. E. KENNEDY

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Herpes Simplex Virusand the Nervous System P. G. E. KENNEDY Postgrad Med J: first published as 10.1136/pgmj.60.702.253 on 1 April 1984. Downloaded from Postgraduate Medical Journal (April 1984) 60, 253-259 Herpes simplex virus and the nervous system P. G. E. KENNEDY M.D., Ph.D., M.R.C.P. Department of Neurological Sciences, St Bartholomew's Hospital, West Smithfield, London ECI Introducdon Both HSV-1 and HSV-2 are capable of infecting Interest in herpes simplex virus (HSV) has in- the human nervous system. The particular neurologi- creased considerably over the last few years, largely cal syndrome caused by HSV depends on a variety of as a result of a more general awareness ofthe possible factors including the age and immune status of the association between HSV-2 and cervical cancer and host, and socio-economic considerations are also the increasing frequency of sexual transmission of important (Nahmias and Roizman, 1973). This arti- HSV-2. Of less general interest is the affinity ofHSV cle will provide an overview of the subject which will for nervous tissues and its ability to cause a variety of be considered from four standpoints: neurological diseases. That HSV can remain latent (1) HSV and clinical neurological disease; within neural tissues is well recognized (Baringer, (2) Latency of HSV in human nervous tissues; 1975). An intriguing question is how the relatively (3) Experimental HSV latency in animal nervous rare acute neurological syndromes, such as HSV tissues; encephalitis and meningitis, are related to the car- (4) Mechanisms involved in HSV latency. riage of latent HSV which is so widespread in human individuals. copyright. HSV is a DNA virus and is one of the four human HSV and clinical neurological disease herpes viruses (the others being varicella-zoster virus, The most important neurological disease caused by cytomegalovirus and Epstein-Barr virus). It has a HSV is an acute encephalitis which is the commonest molecular weight of 99 ± 5 x 10 daltons (Roizman, type of fatal sporadic acute encephalitis occurring in Spear and Kieff, 1973). There are two closely related man (Finelli, 1975). HSV encephalitis has a preva- antigenic subtypes ofHSV: HSV-1 and HSV-2 which lence of 1 case per million per year (Whitley et al., differ in their biological, clinical and epidemiological 1982). Encephalitis due to HSV-1 occurs at all ages http://pmj.bmj.com/ patterns (Nahmias and Roizman, 1973; Kieff, Ba- (Johnson, 1982), whereas HSV-2 encephalitis is chenheimer and Roizman, 1971; Kieff et aL., 1972). usually restricted to neonates in whom it occurs as There is approximately 50%o homology between the part of a disseminated infection. However, a case of DNAs of HSV-l and HSV-2 (Kieff et aL, 1972). HSV-2 encephalitis occurring in a renal transplant HSV-1 usually infects non-genital areas, causing recipient as part of a disseminated HSV-2 infection blisters in the mouth and lips, but it may also infect has been described (Linnemann et al., 1976). The the skin of the upper part ofthe body, the respiratory incidence of a history of 'cold sores' in patients with and gastrointestinal tracts and the eyes (Nahmias and HSV encephalitis is no different from that seen in the on September 30, 2021 by guest. Protected Roizman, 1973). Moreover, it is now recognized that rest of the population (approximately 25%) (Johnson, HSV-1 infects genital sites (Chang, 1977; Wolontis 1982). The mortality rate of HSV encephalitis in and Jeansson, 1977). For example, in the study untreated cases is about 50%, and approximately 50% carried out by Wolontis and Jeansson (1977), HSV-1 of the survivors remain with considerable disability was responsible for 15% of genital infections of all (Johnson, 1982). The disease is almost always local- patients studied; HSV-2 accounted for the remaining ized to the orbito-frontal and temporal lobes which 85% of cases. The type of HSV isolated appeared to show haemorrhagic necrosis, and this localization depend on the age of the patient, with the highest is often unilateral contrasting with the neonatal rates of genital isolation of HSV-1 (30%o) being found encephalitis which produces a diffuse pathology in the 15-24 year age group. HSV-2 infects primarily (Finelli, 1975; Johnson, 1982). Both grey and white the urogenital tract and the skin below the waist matter are involved in the inflammatory process (Johnson, 1982). The mode of transmission ofHSV-1 (Johnson and Mims, 1968). is by respiratory, salivary or sexual contact, whereas It has been suggested that the unique anatomical HSV-2 is transmitted mainly by sexual contact. localization of HSV encephalitis may be a conse- Postgrad Med J: first published as 10.1136/pgmj.60.702.253 on 1 April 1984. Downloaded from 254 P. G. E. Kennedy quence of virus entry by the olfactory pathway with investigated (Saral et al., 1981; Field and Wildy, subsequent spread along the base of the brain 1981) and is now the drug of choice for treatment of (Johnson and Mims, 1968). An alternative theory was HSV encephalitis. Acyclovir is activated specifically proposed by Davis and Johnson (1979) who sug- in HSV-infected cells and has the great advantages of gested that HSV encephalitis may result from virus being non-toxic to normal uninfected cells, and of spread from the trigeminal ganglion which is known inhibiting selectively the HSV-specific DNA poly- to harbour latent HSV in normal individuals (Barin- merase and thymidine kinase (Miranda et al., 1979; ger, 1975; Warren et al., 1977); this point will be Johnson, 1982). Most clinicians in the United discussed later in this article. Evidence for the earlier Kingdom do not routinely perform brain biopsies in view has recently been provided by Esiri (1982) in her case of suspected HSV encephalitis. It is the author's immunohistological study of the distribution of HSV opinion that the advent of acyclovir has made such a antigens in 29 patients dying of HSV encephalitis. position more tenable. It seems justified to treat all HSV antigens were found mainly in the medial and suspected cases of HSV encephalitis with acyclovir at inferior temporal lobes, hippocampus, amygdaloid any early stage ofthe illness without recourse to brain nucleus, olfactory cortex, insula and cingulate gyrus. biopsy in view of the drug's remarkable lack of A significant observation was that viral antigens were toxicity and probably efficacy. HSV causes a number detected in the glial cells ofthe olfactory tract but not of neurological syndromes in addition to encepha- in the trigeminal pathways. These observations litis. The ability of HSV-2 to cause aseptic meningitis supported the view that the route ofHSV infection in in both newborns and adults is well-established this disease is via olfactory rather than trigeminal (Craig and Nahmias, 1973), and in such cases the pathways. virus has been isolated from either the CSF (Stalder Whitley et aL (1982) have recently used the et al., 1973) or the peripheral blood (Craig and technique of DNA restriction enzyme analysis to Nahmias, 1973). HSV-1 has been recovered from study the DNAs of HSV isolates from eight patients the CSF of a patient with ascending myelitis with HSV encephalitis. Isolates were obtained from (Klastersky et al., 1972), and Craig and Nahmias oral and labial sites and from the brains of these (1973) described a case of ascending myelitis prob- patients. The authors concluded that patients with a ably due to HSV-2 which was isolated from vulval combination of oro-labial HSV and HSV encepha- lesions. A lumbosacral radiculomyelopathy syn-copyright. litis may be infected with two different herpes drome has been described in patients with genital simplex viruses and that the encephalitis may be a HSV-2 infections (Caplan, Kleeman and Berg, 1977) consequence of a primary herpetic infection but and Handler et aL (1983) reported a case of HSV-2 could also follow reactivation of latent HSV ge- radiculomyelopathy which responded to adenosine nomes; reinfection by a second virus may also be a arabinoside. factor in the pathogenesis of the encephalitis. It has been suggested that HSV has also been Johnson, Olson and Buescher (1968) pointed out associated with congenital malformations ofthe CNS that the only definitive methods of diagnosing HSV (South et aL, 1969; Johnson, 1982) but definitivehttp://pmj.bmj.com/ encephalitis are by isolation of virus from the brain evidence is lacking. HSV has been implicated in cases or cerebrospinal fluid (CSF) or by demonstration of of trigeminal neuralgia (Finelli, 1975), facial nerve HSV antigens in central nervous system (CNS) cells palsy (McCormick, 1972) and temporal lobe epilepsy using immunofluorescence techniques. They also (Oxbury, Mathews and MacCallum, 1972), but in commented that it is most unusual to make a these various conditions it is not clear whether a definitive diagnosis of non-fatal HSV encephalitis direct cause-and-effect relationship exists between without recourse to brain biopsy. The importance of the diseases and HSV. on September 30, 2021 by guest. Protected obtaining a cerebral biopsy from the clinically involved area has also been emphasized (Johnson, 1982). Latency of HSV in human nervous tissues Successful treatment ofHSV encephalitis is depen- The ability of HSV to produce recurrent infections dent on early diagnosis. Whitley et al. (1977) found in man is well known (reviewed by Baringer, 1975). that adenosine arabinoside (vidarabine) was more For example, spontaneous reactivation of HSV- 1 in effective than placebo administration in biopsy- the form of 'cold sores' on the lips may be produced proven cases of HSV encephalitis. The importance of by a variety of factors including sunlight, stress, early instigation of drug treatment in improving both fever, skin trauma and X-irradiation (Wildy, Field survival and morbidity rates has also been demon- and Nash, 1982).
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