Epidemiology of Herpes Zoster What has Changed

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Regina Allwinn, Sigune Buxbaum, Hans Wilhelm Doerr

Institute for Medical Virology, University Hospital of Frankfurt, Frankfurt am Main, Germany

Herpes zoster (shingles) is an inflammatory neurodermatologic disease, usually localized on a skin segment of the body which is innervated by a sensory nerve. More than 100 years ago, an association between Varicella and herpes zoster has been suggested (see preface of the book). Shingles is a secondary disease to passed Varicella virus (VZV) infection, which latently persists lifelong in the spinal ganglia of the host. The presumably proviral latency is switched to productive infection by several trigger factors resulting in shingles ('girdle rose'). The most important trigger factor is a waning cell-mediated immunity to VZV along a big time interval after primary infection during childhood. Thus, the majority of patients are elderly or those who suffer from immunocompromising diseases. Nevertheless, many case reports remind that herpes zoster occurs also in immunocompetent adolescents and even in children. Numerous clinical observations have elucidated the epidemiology of herpes zoster. Figure 1 displays the viral circulation through the population.

Seroepidemiology

Similar to many other viral infections the spread of VZV can be estimated by serum surveys, which means determination of IgG antibody prevalence in age grouped population samples. IgG antibodies are formed after varicella or sub-clinic VZV infection and persist lifelong in stable titers. Numerous prospective studies or retrospective evaluations have shown that high prevalences are reached already in childhood [1-3]. During the course of life, fluctuating antibody titer is no marker for a subsequent development of herpes zoster. Figure 2 shows serum surveys on different seroconversion titers of VZV-specific IgG antibodies and

Major Causes Herpes Zoster

Herpes zoster up to 20% after 60 years of life.

Causes: waning cell-mediated immunity or provocation like trauma, chemotherapy, UV

Herpes zoster up to 20% after 60 years of life.

Causes: waning cell-mediated immunity or provocation like trauma, chemotherapy, UV

Fig. 1. Natural spread of VZV infection.

Fig. 2. VZV-specific IgG seroprevalence in difference age groups. University Hospital Frankfurt/Main (from reference [1]).
Segmente Zoster

Age groups (years)

Fig. 3. Varicella-zoster antibody seroprevalence (IgA, IgM and IgG), 1999-2004 (n = 5,457 serum samples). University Hospital Frankfurt/Main.

Age groups (years)

Fig. 3. Varicella-zoster antibody seroprevalence (IgA, IgM and IgG), 1999-2004 (n = 5,457 serum samples). University Hospital Frankfurt/Main.

reveals that titer distribution is similar in all age groups [1]. The rapid spread of VZV has not been reduced by improvement of hygiene and social-economic status. For example, in Germany the rise of antibody prevalence throughout life remained constant for 25 years, as compared to a study from 1973 to 1974 [1, 4]. HIV carriers has statistically significant higher prevalences of VZV-specific antibodies, further increasing with progression to AIDS [5]. IgM antibodies and high IgA antibody titers are markers of an active or reactivated VZV infection [6]. Figure 3 shows that - at low percentage - VZV specific IgM and IgA antibodies are present in the serum survey of all age groups and rising in the elderly as expected. This corresponds to the classical scheme given by Hope-Simpson (fig. 4). In contrast to recurrent herpes simplex, VZV reactivations occur throughout life, but they remain sub-clinical for a long time. Only when cell-mediated immunity is reduced, the stimulus of reactivation is high enough to make a breakthrough resulting in a zoster disease [7]. Thus, by serological means, herpes zoster epidemiology can be only approximated. The exact diagnosis of shingles requires clinical evaluation in addition to laboratory markers.

Increasing levels of host resistance

Primary varicella-zoster virus infection Varicella (latent virus goes to sensory ganglia)

Contained reversions u

Contained ra '<ยป \reversions

ct ost

^^ Level of host resistance\^ Critical level of host resistance H

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