Rapid cytotoxic T lymphocyte activation occurs in the draining lymph nodes after cutaneous herpes simplex virus infection as a result of early antigen presentation and not the presence of virus.
(9/98)
Localized cutaneous herpes simplex virus type 1 (HSV-1) infection leads to arming and initial expansion of cytotoxic T lymphocytes (CTLs) in the draining popliteal lymph nodes (PLNs) followed by migration and further proliferation in the spleen. To accurately characterize the sequence of events involved in the activation and generation of anti-HSV CTLs, we used T cell receptor (TCR) transgenic mice specific for the immunodominant epitope from HSV glycoprotein B (gB(498-505)). We describe the detection of the initiation of antigen presentation in the draining lymph nodes by 4-6 h after infection with HSV-1. Analysis of CD69 up-regulation revealed activation of gB-specific CD8(+) T cells by 6-8 h after infection. Furthermore, we show that T cell proliferation begins no sooner than 24 h after activation and is marked by the concurrent appearance of CTL activity in the PLNs. These events are not dependent on the presence of virus in the draining lymph nodes, and suggest a requirement for recruitment of professional antigen-presenting cells to the site of T cell activation. Consequently, we have defined the initiation of the CD8(+) T cell-mediated response to cutaneous HSV-1 infection, demonstrating that the immune response to localized viral infection depends only on the appearance of cells presenting virus-derived antigen and commences with remarkable swiftness. (+info)
Dermal infection with vaccinia virus reveals roles for virus proteins not seen using other inoculation routes.
(10/98)
Previously, we developed a model for testing the virulence and immunogenicity of vaccinia virus (VV) mutants based on the intradermal injection of BALB/c mouse ear pinnae. The model is characterized by a local infection in the inoculated skin without signs of systemic illness, mimicking dermal vaccination with VV. Here a further characterization of this model is presented, including the responses of mice to infectious virus doses as low as 10 p.f.u., a quantification of the infiltrate at the site of infection and use of different virus and mouse strains. The model was then used to compare the pathogenesis of six mutants of VV strain Western Reserve (WR) lacking genes A36R, A40R, A44L, B12R, B13R or B15R with that of appropriate control viruses. All of these genes except B12R and B15R influence the outcome of dermal infection with WR and for A40R and B13R this is the first role that has been reported after infection of mammals. A comparison of new and published results from intradermal and intranasal models is presented, showing that out of 16 gene deletion or insertion mutants of VV, half have phenotypes distinct from controls in only one of these models. Thus, the intranasal and intradermal models are complementary tools for dissecting the genetic basis of VV virulence. (+info)
Papular purpuric rash due to parvovirus B19 with distribution on the distal extremities and the face.
(11/98)
We describe 3 patients who presented with a distinctive clinical picture of the purpuric rash called "gloves-and-socks syndrome" which was characterized by an acral distribution of the rash that involved not only the distal part of the extremities but also the chin and perioral area. Serologic analysis for parvovirus B19 yielded positive results. Parvovirus B19 should be included in the evaluation of febrile purpura. (+info)
Human T lymphotrophic virus-I (HTLV-I) infection in patients with unclassifiable dermatitis in central Kerala, south India: a preliminary study.
(12/98)
OBJECTIVE: We have conducted a preliminary serostudy to confirm the presence of this virus in cases of dermatitis of unknown aetiology and among individuals with sexually transmitted infections (STI) in central Kerala. METHODS: 45 consecutive patients who attended the dermatology clinic of Medical College Kottayam with extensive dermatitis that could not be clinically classified into any known clinical entity and 37 consecutive patients who presented to the sexually transmitted disease (STD) clinic were enrolled for the study. Serum/plasma samples were screened for anti-HTLV-I antibody. Reactive and indeterminate samples were confirmed by an immunoblot. RESULTS: Among 37 STD clinic attendants, none had antibody to HTLV-I while two individuals (4.44%) among the 45 with dermatitis had antibody to HTLV-I. CONCLUSIONS: Our study proves the presence of HTLV-I in a subset of individuals with poorly defined dermatitis in Kerala. Further larger studies are necessary to assess the extent of this problem and its relation to STI in Kerala. (+info)
Cytomegalovirus.
(13/98)
Cytomegalovirus (CMV) is a prevalent viral pathogen. The majority of persons with acute CMV will experience an inapparent infection. Primary CMV infection will cause up to 7 percent of cases of mononucleosis syndrome and will manifest symptoms almost indistinguishable from those of Epstein-Barr virus-induced mononucleosis. CMV, or heterophil-negative mononucleosis, is best diagnosed using a positive IgM serology. Complications of acute CMV infection in immunocompetent persons are rare, except in newborns. The virus usually is spread through close personal contact; transmission risk can be reduced by following simple hygienic and handwashing techniques. Severe illness can occur after reactivation of the latent virus in immunosuppressed persons. The retina is the most common site of CMV-induced pathology in persons with human immunodeficiency virus infection. Advances in the treatment of human immunodeficiency virus infection with highly active antiretroviral therapy (HAART) have decreased the incidence of CMV retinitis but have resulted in a new set of ophthalmologic complications induced by restoration of immune competency and the pro-inflammatory response of the patient to CMV. If HAART restores the patient's CD4 cell count to above 100 to 150 per mm3 (100 to 150 x 10(6) per L), it may preclude lifelong treatment for CMV retinitis. (+info)
A kinetic analysis of immune mediators in the lungs of mice infected with vaccinia virus and comparison with intradermal infection.
(14/98)
The early inflammatory response to a virus may be critical in restricting infection and in shaping the subsequent adaptive immune response. In this study we have examined the early inflammatory response of mice following infection with vaccinia virus (VV) strain Western Reserve (WR). Respiratory challenge of BALB/c mice with VV led to early virus replication in the lung and upper respiratory tract followed by dissemination of virus to other visceral organs and to the brain. The number of inflammatory cells, largely macrophages and T lymphocytes, recovered from bronchoalveolar lavage (BAL) fluid increased markedly during infection and coincided with the expression of CC chemokine ligands (CCL) 3, 2 and 11 and CXC chemokine ligands (CXCL) 1 and 2/3 in BAL. The peak of the inflammatory response occurred around day 10 and declined thereafter. The antiviral cytokines IFN-gamma and TNF-alpha, and the reactive nitrogen intermediate nitric oxide (NO), were also detected in BAL from VV-infected mice. A markedly different inflammatory response was observed after intradermal inoculation of WR into the ear pinnae of mice. Intradermal challenge was followed by highly localized virus replication and by a cellular influx, consisting largely of neutrophils and T lymphocytes, into the dermal compartment of the infected ear. Together these findings highlight differences in the pathogenesis and in the cellular inflammatory response to WR following intranasal and intradermal inoculation of mice. (+info)
The vaccinia virus kelch-like protein C2L affects calcium-independent adhesion to the extracellular matrix and inflammation in a murine intradermal model.
(15/98)
Chordate poxviruses encode several uncharacterized POZ-kelch proteins and three of these are present in Vaccinia virus (VV) strain Western Reserve. VV gene C2L is predicted to encode a protein of 512 amino acid residues with a POZ/BTB domain in the N-terminal region and three kelch motifs in the C-terminal half of the protein. We have identified the C2L gene product as an intracellular protein of 56 kDa and constructed and characterized a VV mutant lacking the C2L gene (v Delta C2L). Compared to wild-type and revertant viruses, v Delta C2L had unaltered growth in vitro, but had a different plaque morphology due to an altered cytopathic effect (CPE) of infected cells. Deleting C2L had no effect on VV-induced formation of actin tails or enhanced cell motility, but affected the development of VV-induced cellular projections and the Ca(2+)-independent cell/extracellular matrix adhesion late during infection. In an intranasal mouse model, C2L did not contribute to virus virulence. However, in an intradermal mouse model, infection with v Delta C2L resulted in larger lesions and more cell infiltration into the infected ears during recovery from infection. Thus, in this model, C2L protein inhibits inflammation and reduces immunopathology. In summary, we found that C2L is not required for virus replication in vitro but contributes to aspects of VV-induced CPE and reduces immunopathology in vivo. (+info)
Viral exanthems.
(16/98)
Viral exanthems are mostly associated with self-limited diseases. However, in some cases diagnosis of an exanthem may be crucial to patients and their contacts. Certain exanthems have fairly characteristic morphology, but in many cases an accurate diagnosis cannot be made on the basis of morphology alone. Historical factors may be helpful when evaluating these patients, specifically their disease contacts, immunization record, previous exanthematous illnesses, and associated prodromal symptoms. Some illnesses are seasonal and this knowledge may be useful. This manuscript reviews a number of common childhood exanthems. We included the most common viral exanthems encountered by primary-care physicians and dermatologists. (+info)