Experimental Zosteriform Herpes Simplex Virus Infection in Mouse Skin

Robinson, T. W. E.; Dover, J. R.

doi:10.1111/j.1365-2133.1972.tb01889.x

Cited by 14 publications

(9 citation statements)

References 10 publications

(4 reference statements)

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“…This effect of inflammation of the skin finds a parallel in our much later observations that in mice mild inflammation is a prerequisite for the production of recurrent herpes lesions (Hill et al, 1978;Harbour et al, 1983). Later sporadic reports have shown that HSV can establish zosteriform lesions in rats (Tanaka & Southam, 1965), mice (Sydiskis & Schultz, 1965;Constantine et al, 1971 ;Dillard et al, 1972;Robinson & Dover, 1972) and man (Music et al, 1971 ;Mok, 1971) without treating the skin with inflammatory agents. Zosteriform spread is also the likely explanation for the occurrence of lesions on the external genitalia of guinea-pigs after intravaginal inoculation of HSV-2 (Stanberry et al, 1982).…”

Section: Discussionmentioning

confidence: 62%

Pathogenesis of Zosteriform Spread of Herpes Simplex Virus in the Mouse

Blyth

Harbour

Hill

1984

Journal of General Virology

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SUMMARYZosteriform spread of herpes simplex virus (HSV) infection occurs after primary inoculation of the skin of both outbred and inbred mice. With HSV type I strain SC 16 few outbred animals died if they were inoculated when 8 weeks old whereas up to 50 of animals died if inoculated when 4 weeks old. However, at either age, zosteriform spread of infection occurred in almost all animals as it did when 4-week-old outbred animals were inoculated with the avirulent strain KOS. Thus, control of zosteriform spread must act by different mechanisms from those controlling the encephalitis which leads to death. During replication in the epidermis virus enters axons and could first be found in sensory ganglia 2 days after inoculation of the skin. Thereafter, it was found in the nerve roots and in skin within the same dermatome but remote from the site of inoculation. When sensory nerves to this latter area were cut during the 4 days after primary inoculation lesions developing as a result of zosteriform spread were either completely inhibited or, with later section, decreased in incidence. Mortality was not affected by such nerve section. Latent infection must be established in neurons serving areas of skin remote from the inoculation site since with HSV-1 strain SC16, recrudescent lesions on the pinna could be induced by stripping the skin of the ear when the original inoculation had been in the skin of the neck. Such recrudescent disease was not demonstrated in animals infected with HSV-1 strain KOS even though this virus efficiently established latent infection in sensory ganglia.

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Section: Discussionmentioning

confidence: 62%

Pathogenesis of Zosteriform Spread of Herpes Simplex Virus in the Mouse

Blyth

Harbour

Hill

1984

Journal of General Virology

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“…It is readily apparent from the zosteriform spread model that lytic replication within neurons results in anterograde transport (32,38,47,48). The arborizing nature of sensory innervation at the surface could result in the deposition of virions at a surface site near, but spatially distinct from, the initial infection site (5,7,58).…”

Section: Vol 74 2000mentioning

confidence: 99%

Replication of Herpes Simplex Virus Type 1 within Trigeminal Ganglia Is Required for High Frequency but Not High Viral Genome Copy Number Latency

Thompson

Sawtell

2000

J Virol

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The replication properties of a thymidine kinase-negative (TK ؊ ) mutant of herpes simplex virus type 1 (HSV-1) were exploited to examine the relative contributions of replication at the body surface and within trigeminal ganglia (TG) on the establishment of latent infections. ؊ in the absence of significant replication within the TG resulted in a modest increase in the number of latent sites. Importantly, these latently infected neurons displayed a wild-type latent-genome copy number profile, with some neurons containing hundreds of copies of the TK ؊ mutant genome. As expected, the replication of the TK ؊ mutant appeared to be blocked prior to DNA replication in most ganglionic neurons in that (i) virus replication was severely restricted in ganglia, (ii) the number of neurons expressing HSV proteins was reduced 30-fold compared to the rescued isolate, (iii) cell-to-cell spread of virus was not detected within ganglia, and (iv) the proportion of infected neurons expressing late proteins was reduced by 89% compared to the rescued strain. These results demonstrate that the viral TK gene is required for the efficient establishment of latency. This requirement appears to be primarily for efficient replication within the ganglion, which leads to a sixfold increase in the number of latent sites established. Further, latent sites with high genome copy number can be established in the absence of significant virus genome replication in neurons. This suggests that neurons can be infected by many HSV virions and still enter the latent state.

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“…A short period of viral replication within infected sensory ganglia is concomitant with the establishment of a nonproductive latent infection (22). During acute infection, HSV may reemerge from the nervous system and cause disease within the same dermatome at a location distal from the initial site of infection (4,7,18,24,32). This phenomenon, termed zosteriform spread, has been shown in mouse models to progress from flank to flank, snout to eye, mouth to eye, and neck to pinna.…”

mentioning

confidence: 99%

Herpes Simplex Virus Type 1 Corneal Infection Results in Periocular Disease by Zosteriform Spread

Summers

Margolis

Leib

2001

J Virol

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In humans and animal models of herpes simplex virus infection, zosteriform skin lesions have been described which result from anterograde spread of the virus following invasion of the nervous system. Such routes of viral spread have not been fully examined following corneal infection, and the possible pathologic consequences of such spread are unknown. To investigate this, recombinant viruses expressing reporter genes were generated to quantify and correlate gene expression with replication in eyes, trigeminal ganglia, and periocular tissue. Reporter activity peaked in eyes 24 h postinfection and rapidly fell to background levels by 48 h despite the continued presence of viral titers. Reporter activity rose in the trigeminal ganglia at 60 h and peaked at 72 h, concomitant with the appearance and persistence of infectious virus. Virus was present in the periocular skin from 24 h despite the lack of significant reporter activity until 84 h postinfection. This detection of reporter activity was followed by the onset of periocular disease on day 4. Corneal infection with a thymidine kinase-deleted reporter virus displayed a similar profile of reporter activity and viral titer in the eyes, but little or no detectable activity was observed in trigeminal ganglia or periocular tissue. In addition, no periocular disease symptoms were observed. These findings demonstrate that viral infection of periocular tissue and subsequent disease development occurs by zosteriform spread from the cornea to the periocular tissue via the trigeminal ganglion rather than by direct spread from cornea to the periocular skin. Furthermore, clinical evidence is discussed suggesting that a similar mode of spreading and disease occurs in humans following primary ocular infection.

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Experimental Zosteriform Herpes Simplex Virus Infection in Mouse Skin

Cited by 14 publications

References 10 publications

Pathogenesis of Zosteriform Spread of Herpes Simplex Virus in the Mouse

Pathogenesis of Zosteriform Spread of Herpes Simplex Virus in the Mouse

Replication of Herpes Simplex Virus Type 1 within Trigeminal Ganglia Is Required for High Frequency but Not High Viral Genome Copy Number Latency

Herpes Simplex Virus Type 1 Corneal Infection Results in Periocular Disease by Zosteriform Spread

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