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HSV-1 Infection (hsv-1 + infection)
Selected AbstractsBone marrow-derived cells expand memory CD8+ T,cells in response to viral infections of the lung and skinEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2006Gabrielle Abstract While naive CD8+ T,cells have been shown to require bone marrow-derived dendritic cells (DC) to initiate immunity, such a requirement for memory CD8+ T,cells has had limited assessment. By generating bone marrow chimeras that express the appropriate antigen-presenting molecules on either radiation-sensitive bone marrow-derived or radiation-resistant non-bone marrow-derived compartments, we showed that both primary and secondary immune responses to influenza virus infection of the lung were initiated in the draining LN. This required cells of bone marrow origin, most likely DC, for optimal expansion within the secondary lymphoid compartment. This was similarly the case with HSV-1 infection of the skin. As Langerhans cells are radioresistant, unlike other DC populations, these studies also demonstrate that the radiosensitive DC responsible for secondary expansion of HSV-specific memory are not Langerhans cells. [source] The Role of DNA Recombination in Herpes Simplex Virus DNA ReplicationIUBMB LIFE, Issue 8 2003Dianna Wilkinson Abstract In many organisms the processes of DNA replication and recombination are closely linked. For instance, in bacterial and eukaryotic systems, replication forks can become stalled or damaged, in many cases leading to the formation of double stranded breaks. Replication restart is an essential mechanism in which the recombination and repair machinery can be used to continue replication after such a catastrophic event. DNA viruses of bacteria such as lambda and T4 also rely heavily on DNA recombination to replicate their genomes and both viruses encode specialized gene products which are required for recombination-dependent replication. In this review, we examine the linkage between replication and recombination in the eukaryotic pathogen, Herpes Simplex Virus Type 1 (HSV-1). The evidence that recombination plays an intrinsic role in HSV-1 DNA replication and the infection process will be reviewed. We have recently demonstrated that HSV-1 encodes two proteins which may be analogous to the lambda phage recombination system, Red ,and ,. The HSV-1 alkaline nuclease, a 5' to 3' exonuclease, and ICP8, a single stranded DNA binding protein, can carry out strand annealing reactions similar to those carried out by the lambda Red system. In addition, evidence suggesting that host recombination proteins may also be important for HSV-1 replication will be reviewed. In summary, it is likely that HSV-1 infection will require both viral and cellular proteins which participate in various pathways of recombination and that recombination-dependent replication is essential for the efficient replication of viral genomes. IUBMB Life, 55: 451-458, 2003 [source] Peptide based vaccine design: Synthesis and immunological characterization of branched polypeptide conjugates comprising the 276,284 immunodominant epitope of HSV-1 glycoprotein DJOURNAL OF PEPTIDE SCIENCE, Issue 3 2002Gábor Mez Abstract The importance of the length and conjugation site of a protective epitope peptide (276SALLEDPVG284) from glycoprotein D of herpes simplex virus in branched polypeptide conjugates has been investigated. A new set of peptides, with a single attachment site and truncated sequences, was prepared. The immunogenicity of conjugates and the specificity of antibody responses elicited were investigated in BALB/c, C57/Bl/6 and CBA mice. It was found that the covalent coupling of the peptide comprising the 276,284 sequence of gD through its Asp residue at position 281 did not influence the immunogenic properties of the epitope, while involvement of the side chain of Glu at position 280 almost completely abolished immunogenicity. These results clearly indicated that the conjugation site of the epitope peptide influenced the intensity and specificity of antibody responses. Comparison of the immunological properties of conjugates containing truncated gD peptides revealed the presence of two epitopes within the 276,284 region. One of the proposed epitopes is situated at the N -terminal (276,281) region, while the other is located at the C -terminal end of the sequence (279,284). Binding data demonstrated that some of the peptides comprising these epitopes induced gD-specific responses in their conjugated form and also elicited an immune response that conferred protection against lethal HSV-1 infection. The correlation of peptide- and gD-specific antibody responses with the protective effect of the immune response is discussed. Copyright © 2002 European Peptide Society and John Wiley & Sons, Ltd. [source] Herpes simplex virus type 1 dysregulates anti-fungal defenses preventing monocyte activation and downregulating toll-like receptor-2MICROBIOLOGY AND IMMUNOLOGY, Issue 12 2008Claudio Cermelli ABSTRACT We investigated the interplay occurring between pathogens in the course of dual infections, using an in vitro model in which the THP-1 monocytic cell line is first infected with HSV-1 and then exposed to Ca or Cn. These three pathogens share some pathogenic features: they cause opportunistic infections, target macrophages and are neurotropic. Here, we show that HSV-1-infected THP-1 cells exhibited augmented phagocytosis against the two opportunistic fungi but reduced capability to counteract fungal infection: the better ingestion by monocytes was followed by facilitated fungal survival and replication. Reduced IL-12 production was also observed. Cytofluorimetric analysis showed that HSV-1-infected monocytes exhibit: (i) downregulated TLR-2 and TLR-4, critical structures in fungal recognition; (ii) reduced expression of CD38 and CD69, known to be important markers of monocyte activation; and (iii) enhanced expression of apoptosis and necrosis markers, in the absence of altered cell proliferation. Overall, these findings imply that HSV-1 infection prevents monocyte activation, thus leading to a significant dysfunction of the monocyte-mediated anti- Candida response; HSV-1 induced apoptosis and necrosis of monocytes further contribute to this impairment. [source] Proteomic analysis of cells in the early stages of herpes simplex virus type-1 infection reveals widespread changes in the host cell proteomePROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 15 2009Robin Antrobus Abstract During infection by herpes simplex virus type-1 (HSV-1) the host cell undergoes widespread changes in gene expression and morphology in response to viral replication and release. However, relatively little is known about the specific proteome changes that occur during the early stages of HSV-1 replication prior to the global damaging effects of virion maturation and egress. To investigate pathways that may be activated or utilised during the early stages of HSV-1 replication, 2-DE and LC-MS/MS were used to identify cellular proteome changes at 6,h post infection. Comparative analysis of multiple gels representing whole cell extracts from mock- and HSV-1-infected HEp-2 cells revealed a total of 103 protein spot changes. Of these, 63 were up-regulated and 40 down-regulated in response to infection. Changes in selected candidate proteins were verified by Western blot analysis and their respective cellular localisations analysed by confocal microscopy. We have identified differential regulation and modification of proteins with key roles in diverse cellular pathways, including DNA replication, chromatin remodelling, mRNA stability and the ER stress response. This work represents the first global comparative analysis of HSV-1 infected cells and provides an important insight into host cell proteome changes during the early stages of HSV-1 infection. [source] 2213: Herpetic keratitis: Herpes simplex virus versus hostACTA OPHTHALMOLOGICA, Issue 2010G VERJANS Herpes simplex virus type 1 (HSV-1) is an endemic virus worldwide that causes ocular disease in a limited but significant number of infected persons. Corneal HSV-1 infection is clinically classified into herpetic epithelial keratitis (HEK) and herpetic stromal keratitis (HSK). HEK is an acute inflammation and results from viral toxicity of infected corneal epithelial cells. In contrast, HSK is characterized as a chronic immunopathogenic disease in which tissue injury and eventually blindness is due to the complex interplay between cells of the innate and adoptive immune response to viral antigens expressed in the corneal tissue. Studies performed on the experimental HSK mouse model greatly improved our understanding of the pathogenesis of HSK. This talk will recapitulate current insights on the virus-host interactions involved in the initiation and perpetuation of herpetic keratitis in mice and men. [source] | ||||||||||||||||