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Herpesviruses J Clin Pathol: first published as 10.1136/jcp.32.9.859 on 1 September 1979. Downloaded from Journal of Clinical Pathology, 1979, 32, 859-881 Herpesviruses MORAG C. TIMBURY' AND ELIZABETH EDMOND2 From the 'Department of Bacteriology, Royal Infirmary, Glasgow and the 2Regional Virus Laboratory, City Hospital, Greenbank Drive, Edinburgh, UK Herpesviruses are ubiquitous in both human and tion (Plummer et al., 1970) or microneutralisation animal populations (Plummer, 1967). The four tests (Pauls and Dowdle, 1967) are often used for human herpesviruses are herpes simplex (HSV), this, but differentiating the two types of virus today varicella-zoster (VZ), cytomegalovirus (CMV), and can probably be done more easily by biochemical Epstein-Barr (EBV) viruses, and all exhibit the prop- methods. Thus the DNA of the viruses can be dis- erty, rare among human pathogenic viruses, of tinguished by restriction enzyme analysis (Skare et remaining latent within the body after primary infec- al., 1975). Similarly, many of the virus polypeptides tion. Latent virus persists for many years-probably produced in infected cells by the two types of virus throughout life-and in some patients reactivates to can be distinguished by polyacrylamide gel electro- cause secondary or recurrent infections. Human phoresis (Courtney and Powell, 1975). herpesviruses can almost be regarded as part of the commensal flora, and certainly HSV is present in LABORATORY DIAGNOSIS the saliva of healthy people from time to time HSV-1 infections are most rapidly diagnosed by (Douglas and Couch, 1970). The viruses exhibit a isolation of the virus in cell cultures such as BHK21 remarkably successful parasitism since the upset to or RK1 3 cells (Grist et al., 1979). The virus causes a copyright. the host is minimal or, more often, absent. Like all rapid and characteristic CPE, and identification can herpesviruses, the four human viruses have identical subsequently be confirmed by neutralisation test. particles with a striking morphology (Fig. 1). Never- Primary infection can be diagnosed serologically by theless, they differ considerably in biological and demonstration of a rising titre or sometimes by high pathogenic properties, and it is these that will be stationary titres of antibody in complement fixation described and compared in this review. tests. Cross reactions with VZ virus may make interpretation difficult, but neutralisation tests are Herpes simplex virus usually specific (Grist et al., 1978). Recurrent infec- http://jcp.bmj.com/ tions do not usually cause either a rise in titre or HSV is the most studied and best understood of the diagnostically high titres of antibody. If laboratory human herpesviruses. Easy to cultivate in cell diagnosis is required, isolation should be attempted. cultures, it produces a rapid and characteristic cyto- pathic effect (CPE). There are two types of HSV: EPIDEMIOLOGY type I (HSV-l) and type 2 (HSV-2). These differ in Infection with HSV-1 is virtually universal. The most their sites of infection since HSV-1 infects head common route of infection is close personal contact, on September 26, 2021 by guest. Protected and neck, whereas HSV-2 infects the skin below the such as kissing, when virus is transmitted via infected waist and most often causes lesions on the genitalia. mouth secretions. Infection is usually acquired The difference in site is not absolute, and Smith et al. during the first three years of life, the incidence of (1976) have found that 22% of genital lesions in antibody rising steadily throughout childhood to female patients were due to HSV-1. HSV-2 differs show a second peak during adolescence (Smith et from HSV-1 in several properties although the al., 1967). Smith and her co-workers found that 84% viruses are genetically very similar (Kieff et al., 1972). of people aged between 30 and 39 years had HSV-1 HSV-1, for example, grows to higher titre in cell antibody. HSV-2 is usually sexually transmitted cultures, is more thermostable, and produces a (Astruc, 1754) and is less common than HSV-1. recognisably different CPE to HSV-2 (Plummer et Nevertheless, HSV-2 infection is not rare, and sug- al., 1968; 1970). Despite a considerable degree of gestions that it may play a role in cervical cancer cross-neutralisation, the viruses can be distinguished have kept interest in this virus at a high level (Naib, serologically (Schneweis, 1967). Kinetic neutralisa- 1966; Rawls et al., 1970). The association is not yet proven, but HSV-2 shows oncogenic potential in Received for publication 15 May 1979 vitro in that it transforms cultures of rodent embryo 859 J Clin Pathol: first published as 10.1136/jcp.32.9.859 on 1 September 1979. Downloaded from 860 Morag C. Timbury and Elizabeth Edmond Fig. 1 Herpes simplex virus particle x 108 000. Photograph by Dr E. A. C. Follett. copyright. Reproduced with permission from Notes on Medical Virology by M. C. Timbury, Sixth edition. Churchill Livingstone, 1978. cells (Duff and Rapp, 1971; Macnab, 1974). A focus associated with considerable constitutional dis- of HSV-2 transformed cells is shown in Figure 2. turbance. Babies born to mothers with a primary HSV-2 infection late in pregnancy sometimes develop PRIMARY HSV INFECTIONS generalised HSV-2 infection (Nahmias et al., 1967). Primary infections with HSV-1 are usually symptom- Not all cases of neonatal herpes are due to HSV-2; http://jcp.bmj.com/ less, but when disease is produced this most often some are due to HSV-1, and in them the source of takes the form of acute gingivostomatitis with pain- infection is-probably most often a HSV-1 lesion in ful membranous ulcers in the mouth (BurneL and the mother (Quilligan and Wilson, 1951; Hanshaw Williams, 1939). Vesicles are sometimes produced on and Dudgeon, 1978) or, in one instance, probably other areas of the skin, the head or neck being the the father (Linnemann et al., 1978). Clinically, neo- commonest sites. Sometimes the eye is affected, natal herpes is generally a severe disease with a high giving rise to keratoconjunctivitis (Mintz, 1976). mortality rate. The infection is disseminated with a on September 26, 2021 by guest. Protected Primary herpes can produce a surprisingly large vesicular rash and signs of visceral involvement due number of different diseases. For example, infection to hepatoadrenal necrosis (Hass, 1935). Respiratory of the finger can mimic a painful whitlow (Adamson, distress and bleeding are common features, but some- 1909). This is an occupational hazard of anaesthetists times signs of CNS disturbance such as convulsions and nurses whose fingers may become contaminated and raised intracranial pressure dominate the clinical with virus-containing throat secretions from patients picture (Hanshaw and Dudgeon, 1978). Primary (Stern et al., 1959). HSV-1 may superinfect ecze- infection with HSV-1 can become disseminated in matous skin to cause Kaposi's varicelliform eruption previously healthy adults, but this is very rare (Kaposi, 1895; Lynch, 1945), a condition that may (Kipping and Downie, 1948; Juel-Jensen, 1970). be severe with a case fatality rate of up to 50% Generalised herpes presenting as acute hepatitis in an (Mintz, 1976). HSV-2, the cause of genital herpes, adult has also been described (Francis et al., 1972). produces vesicles progressing to ulceration on ex- ternal genitalia or the anal region. The cervix is LATENCY probably quite often involved in genital herpes, and Both HSV-1 and HSV-2 become latent in ganglia Willcox (1968) has described necrotic cervicitis after primary infection. With HSV-1 this is most J Clin Pathol: first published as 10.1136/jcp.32.9.859 on 1 September 1979. Downloaded from Herpesviruses 861 copyright. Fig. 2 Focus of rat embryo cells transformed by type 2 herpes simplex virus. Photograph by Dr J. C. Macnab. often the trigeminal ganglia (Bastian et al., 1972; REACTIVATION Baringer and Swoveland, 1973) from which virus can HSV-1 reactivations are either symptomless (Douglas be recovered in 60% of cadavers by co-cultivation and Couch, 1970) or cause the familiar cold sores at with susceptible cells (Warren et al., 1977). The state mucocutaneous junctions around the mouth and http://jcp.bmj.com/ of the virus in the ganglia is unknown. To recover nostrils. Recurrent infection seems to be due to virus virus from ganglia requires prolonged co-cultivation reactivation in ganglia with centrifugal spread down of ganglion explants with susceptible cells; yet HSV sensory nerves to cause lesions in areas of skin sup- is a fast-growing virus which normally produces a plied by the nerves (Goodpasture, 1929). Recurrent rapid CPE in cell culture. This suggests that HSV is infection sometimes involves the cornea (presumably not present in ganglia as free infectious virus. It is via the ophthalmic nerve from the trigeminal tempting to speculate that the virus DNA may be ganglion) to cause dendritic ulceration with the risk on September 26, 2021 by guest. Protected integrated into the chromosomes of the neurones or of progressive damage to the eye (Jones, 1958; Norn, other ganglion cells in the form of a provirus, but 1970). Like HSV-1, HSV-2 infection on the genitalia there is no evidence at present to support this. The may become recurrent (Legendre, 1853; Hutfield, mechanism of reactivation of latent virus and its 1967; Parker and Banatvala, 1967). The most severe subsequent neural spread to produce lesions in the of all herpes diseases is acute necrotising encephalitis appropriate area of skin is also unknown. Recently, (Smith et al., 1941; Olson et al., 1967; Adams and latent HSV-1 has also been demonstrated in the Jennett, 1967). Although the origin of the virus in superior cervical and vagus ganglia (Warren et al., this disease is uncertain, it is probably more often 1978). Linnemann et al. (1978) have shown that due to reactivation than to primary infection.
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