Search PubMed⌕ Search

Biomedical subjects

W A Blyth

Publications and source records attributed to W A Blyth.

At least 37 records · Page 2Linked to original sources
PubMed1985

The effects of cyclosporin A on the induction, expression and regulation of the immune response to herpes simplex virus.

Investigations were conducted to determine the effect of cyclosporin A (CsA) on the delayed type hypersensitivity (DTH) and antibody response of mice to Herpes simplex virus (HSV). Given only at the time of priming, the drug had little effect on the subsequent DTH response in mice receiving a 'DTH immunogenic' inoculation regime. However, CsA restored normal responsiveness in groups receiving a 'DTH tolerogenic' regime implying the abrogation of T suppressor (Ts) cells. Ts cell induction was insensitive to cyclophosphamide. Antibody responses were not suppressed after giving CsA with either of these regimes and enhancement was shown in some groups. DTH was substantially reduced by CsA when the drug was given repeatedly between the time of priming and challenge, or when previously primed mice received the drug shortly before challenge.

Animals↗
PubMed1984

Pathogenesis of zosteriform spread of herpes simplex virus in the mouse.

Zosteriform spread of herpes simplex virus (HSV) infection occurs after primary inoculation of the skin of both outbred and inbred mice. With HSV type 1 strain SC16 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.

Acute Disease↗
PubMed1984

Lipopolysaccharide-induced suppressor cells for delayed-type hypersensitivity to herpes simplex virus: nature of suppressor cell and effect on pathogenesis of herpes simplex.

Treatment of mice with LPS at the time of priming with herpes simplex virus type 1 (HSV1) causes the preferential activation of virus-specific T suppressor (Ts) cells. These Ts cells can transfer suppression to the efferent limb of a DTH response. Priming under these conditions is associated with enhanced cell-recruitment to the inoculation site, but had no effect on virus clearance. The induction of suppression was abrogated by pretreatment of mice with cyclophosphamide or indomethacin. LPS had no effect on the antibody response to HSV1 during acute infection, although treated mice showed a raised antibody titre one month after inoculation. Susceptible mice inoculated with HSV1 and given LPS showed protection, both from lethal herpes encephalitis and from demyelination within the CNS as reflected by ear paralysis. These results imply that, during some stages of acute infection, T cell effector mechanisms may themselves mediate tissue damage. At such times, Ts cells may perform a beneficial role leading to a reduction in pathology.

Animals↗
PubMed1983

Ocular infection with herpes simplex virus in nonimmune and immune mice.

In a detailed study of ocular infection by herpes simplex virus (HSV) type 1 in mice, the course and signs of eye disease were investigated and compared in primary and secondary infection using slit-lamp examination, culture of the tear film, and monitoring of the blink reflex. Response to primary inoculation ranged from subclinical infection to severe keratitis. Compared with conjunctival scarification, corneal scarification resulted in more frequent and severe eye disease and signs of CNS infection. Previous infection in the skin of the contralateral ear considerably modified subsequent infection of the eye so that signs of disease occurred earlier, were limited to dendritic keratitis with some stromal involvement, and were largely reversible. The mouse seems to be a suitable animal for studying ocular infection with HSV.

Animals↗
PubMed1983

Recurrence of herpes simplex in the mouse requires an intact nerve supply to the skin.

The nerves supplying the pinna of the ear of mice latently infected in the 2nd and 3rd cervical ganglia were sectioned. Immediately after neurotomy, or some days later, the denervated ears were stripped with cellophane tape to induce recurrent disease. The cervical ganglia and skin of the ears were tested for the presence of infectious virus at different times after neurotomy. Nerve section induced a low incidence of reactivation of virus in ganglia. After neurotomy, infectious virus was isolated from the skin very rarely and recurrent disease was not seen.

Animals↗
PubMed1983

Prostaglandins enhance intercellular adhesion of Vero cells infected with herpes simplex virus.

The effect of prostaglandins (PGs) and cyclic nucleotides on adherence between uninfected Vero cells or between uninfected cells and cells infected with wild-type or syncytial strains of herpes simplex virus (HSV) was studied. In the absence of serum, PGE2 increased adhesion between uninfected cells whereas PGF2 alpha decreased it. However, both PGE2 and PGF2 alpha increased adhesion between cells infected with HSV and uninfected cells. Moreover, dibutyryl cyclic AMP increased adhesion between uninfected cells and cells infected with HSV, whereas dibutyryl cyclic GMP decreased it.

Animals↗
PubMed1983

Recurrent herpes simplex in the mouse: inflammation in the skin and activation of virus in the ganglia following peripheral stimulation.

The originally infected ear of mice latently infected in the cervical ganglia with herpes simplex virus (HSV) was treated with one of five stimuli: stripping with cellophane tape, irradiation with u.v. light, or the application of xylene, dimethyl sulphoxide (DMSO) or retinoic acid. Each of these stimuli induced the appearance of infectious virus in the ganglia 1 to 5 days later, most frequently after 1 to 3 days. Virus was also isolated from the treated ears, most frequently 3 to 5 days after stimulation. In a proportion of mice treated with cellophane tape stripping, xylene, retinoic acid or DMSO, clinical recurrent disease was observed, although in the case of DMSO this proportion was low. Some of the physiological changes induced in the skin by the five stimuli were studied. Treatment with DMSO, cellophane tape stripping or xylene induced almost immediate inflammation in the skin as judged by extravasation of Evans blue dye. Studies with inhibitors suggested that this was mediated by a neurogenic factor together with histamine or 5-hydroxytryptamine, or both of these. In addition, with the exception of mice treated with DMSO, the levels of prostaglandins of the E and F classes in the skin of the ear were elevated 1 to 3 days after treatment. These results are discussed with reference to the mechanisms by which recurrent herpetic disease develops.

Animals↗
PubMed1983

Corneal sensitivity and substance P in experimental herpes simplex keratitis in mice.

Experimental herpes simplex keratitis in the mouse produced a rapid fall in both corneal sensitivity and levels of corneal substance P (SP). This finding supports the association of SP with sensory neurones and shows that such levels can be used as an indication of damage to neurones resulting, for example, from infection with HSV. However, the delay in recovery of SP compared to the more rapid and complete recovery of sensitivity suggests that SP in the cornea is not directly involved in mediation of the blink reflex.

Animals↗
PubMed1982

Substance P in the mouse cornea: effects of chemical and surgical denervation.

The substance P content of the cornea of the adult mouse has been determined by radioimmunoassay. Sympathectomy did not reduce corneal substance P levels. However substance P levels were reduced by 42% following surgical denervation and by 80% following neonatal capsaicin treatment, suggesting that corneal substance P is contained in the peripheral terminals of small diameter sensory neurones. In some mice capsaicin treatment reduced corneal sensitivity; it also resulted in marked corneal vascularization. These effects could not be ascribed to the reduction in corneal substance P.

Animals↗
PubMed1982

Cell-mediated immunity in mice with primary, secondary and latent herpes simplex virus infection.

Cell mediated immunity was studied by a cytopathic effect inhibition assay in mice infected in the ear with herpes simplex virus type 1 (HSV 1). Activity appeared rapidly, reaching a high level 6 days after primary infection. It had fallen 10 days after infection and was undetectable during latency, 3-5 weeks after infection. The activity reappeared even more rapidly and strongly after reinoculation with the virus, but stimuli designed to induce recurrent disease did not induce clinical disease in the animals and no activity was detected in them. The activity, which was specific for HSV, was shown to be mediated by T-lymphocytes.

Animals↗
PubMed1982

Neutralising antibody in mice with primary and recurrent herpes simplex virus infection.

Neutralising antibody was studied in mice infected in the ear with herpes simplex virus type 1. Antibody was detected six days after infection and after one month it had reached titres which subsequently varied little. Geometric group mean titres were doubled by reinoculation of virus whereas recurrent disease induced by trauma did not change them (although titres did change in some individual animals). Mean titres in mice which had had unequivocal signs of primary disease were twice as high as in those which had not, and the frequency of recurrent disease in response to trauma in the former animals was greater than in the latter. A reduction in the frequency of induced recurrent disease was seen if the application of trauma was delayed for some time after the establishment of latency. Hyperimmunisation increased mean titres tenfold. If given soon after primary infection it reduced the frequency of induced recurrent disease but if its administration was delayed then the frequency was increased.

Animals↗
PubMed1982

Spread of virus and distribution of latent infection following ocular herpes simplex in the non-immune and immune mouse.

In both non-immune and immune mice infected with herpes simplex virus the incidence of latent infection of the trigeminal ganglion was related to the severity of ocular virus infection. During primary infection, virus was shown to travel via the ophthalmic part of the ganglion to reach the brainstem, from where centrifugal spread resulted in latent infection of neurones in the trigeminal ganglion which did not serve the site of inoculation. Primary infection also resulted in latent infection of the superior cervical ganglion. Shedding of virus occurred rarely in the tears of animals which had recovered from primary disease. In immune mice, spread of virus resulted in a much lower incidence of latent infection and that occurred only in ophthalmic neurones.

Animals↗
PubMed1982

Ocular herpes simplex and the establishment of latent infection.

Latent infection of the trigeminal ganglion following ocular and labial herpes simplex in the mouse was investigated. Latent infection of the ophthalmic part of the trigeminal ganglion followed subclinical ocular infection. When primary infection resulted in severe eye disease, latent infection was subsequently demonstrated not only in ophthalmic parts of the ganglion but also in parts which did not serve the eye. Primary infection of the lip resulted in latent infection of the mandibular part of the trigeminal ganglion, but also of maxillary and ophthalmic parts. Previous infection by herpes simplex virus in a non-ocular site necessitated a hundred-fold increase in the amount of virus required to initiate keratitis which resulted in a much lower incidence of latent infection and only in the ophthalmic part of the ganglion. The results are interpreted to explain how latent infection of the ophthalmic part may precede and provide a source of virus for symptomatic eye disease. Such latent infection is most likely to arise from previous subclinical ocular infection or primary infection in a non-ocular site.

Animals↗
PubMed1981

Acute and recurrent herpes simplex in several strains of mice.

Acute and recurrent herpes simplex was studied after infection in the ear of two outbred and five inbred strains of mice. In all strains tested there was clinical evidence of infection, and a proportion of the mice became latently infected in the cervical ganglia. Six weeks after infection, when attempts were made to induce recurrent desease by stripping the ears of the mice with cellophange tape, a proportion of animals of each strain developed recurrent disease, characterized by erythema in the skin. At monthly intervals thereafter, the ears were stripped again and, on each occasion, a proportion of the animals developed recurrent disease, with the exception of Balb/c mice. The different reaction of Balb/c and other inbred strains might prove useful in studies on the mechanism of control of recurrent herpes simplex.

Acute Disease↗