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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5 || Follicle and follicular cells research abs 1 || Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs

J Dermatol Sci. 2002 Sep;29(3):201-5.
Expression of inducible nitric oxide synthase in skin lesions of acute herpes zoster.

Lim YJ, Chang SE, Choi JH, Sung KJ, Bahk JH, Do SH, Lee DS.

Department of Anesthesiology and Clinical Research Institute, Seoul National University Hospital, 28 Yongon-dong, Chongno-gu, 110-744 Seoul, South Korea.

Histopathologically, the skin lesions of acute herpes zoster (AHZ) are characterized by epidermal necrotic vesicles with inflammation. Nitric oxide (NO) is generated from L-arginine by nitric oxide synthase (NOS), and immune inflammation involves the activation of NOS in both effector cells and target cells. NO can cause apoptosis and necrosis of target cells such as keratinocytes. We proposed that a large burst of NO in AHZ may cause the epidermal necrosis. Skin biopsies were taken from 13 patients with AHZ. The expression of inducible-type NOS (iNOS) was examined by immunoperoxidase staining and reverse transcription-polymerase chain reaction (RT-PCR). In the skin specimen of AHZ, moderate-to-strong staining for iNOS was observed in inflammatory cells and necrotic keratinocytes, while weak staining was observed in non-necrotic peripheral keratinocytes. RT-PCR using skin specimen of AHZ corroborated the immunoperoxidase findings, yielding bright bands for iNOS. Normal control skin showed minimal or negative expression both by immunoperoxidase stains and RT-PCR. Increased expression of iNOS is consistent with the hypothesis that high level of NO induced by iNOS may be associated with the epidermal necrosis with inflammation seen in the skin lesions of AHZ.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12234710&dopt=Abstract

EMBO J. 2002 Sep 16;21(18):4989-97.
Visualization of parental HSV-1 genomes and replication compartments in association with ND10 in live infected cells.

Sourvinos G, Everett RD.

MRC Virology Unit, Church Street, Glasgow G11 5JR, UK.

The relative location of active and repressed genes within the nucleus is becoming recognized as a significant factor in the control of gene expression. We have developed systems to visualize parental and replicated herpes simplex virus type 1 (HSV-1) amplicon genomes in association with PML nuclear bodies (ND10) in live cells. Plasmids containing viral replication and packaging signals, a gene expressing enhanced yellow fluorescent protein linked to the tetracycline repressor DNA binding domain and 14 copies of the tetracycline operator sequence were used to produce amplicon genomes packaged into normal viral particles. The frequency of the juxtaposition of viral genomes and ND10 was substantially increased by inclusion of an active HSV-1 Early gene transcription unit, indicating that the association is neither random nor passive. Furthermore, the ND10-associated genomes preferentially progressed to form viral replication compartments. Thus, active viral transcription contributes to the efficiency of viral genome association with ND10, and this in turn increases the probability that the genome will engage in active DNA replication. These studies in live cells provide a novel insight into virus-ND10 interactions and provide compelling visualization of their functional relevance.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12234938&dopt=Abstract

J Biol Chem. 2002 Nov 15;277(46):44292-9. Epub 2002 Sep 15.
Interaction of HCF-1 with a cellular nuclear export factor.

Mahajan SS, Little MM, Vazquez R, Wilson AC.

Department of Microbiology and the Kaplan Comprehensive Cancer Center, New York University School of Medicine, New York, New York 10016, USA.

HCF-1 is a cellular protein required by VP16 to activate the herpes simplex virus (HSV) immediate-early genes. VP16 is a component of the viral tegument and, after release into the cell, binds to HCF-1 and translocates to the nucleus to form a complex with the POU domain protein Oct-1 and a VP16-responsive DNA sequence. This VP16-induced complex boosts transcription of the viral immediate-early genes and initiates lytic replication. In uninfected cells, HCF-1 functions as a coactivator for the cellular transcription factors LZIP and GABP and also plays an essential role in cell proliferation. VP16 and LZIP share a tetrapeptide HCF-binding motif recognized by the beta-propeller domain of HCF-1. Here we describe a new cellular HCF-1 beta-propeller domain binding protein, termed HPIP, which contains a functional HCF-binding motif and a leucine-rich nuclear export sequence. We show that HPIP shuttles between the nucleus and cytoplasm in a CRM1-dependent manner and that overexpression of HPIP leads to accumulation of HCF-1 in the cytoplasm. These data suggest that HPIP regulates HCF-1 activity by modulating its subcellular localization. Furthermore, HPIP-mediated export may provide the pool of cytoplasmic HCF-1 required for import of virion-derived VP16 into the nucleus.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235138&dopt=Abstract

Nucleic Acids Res. 2002 Sep 15;30(18):4009-21.
Sequence analysis of bacteriophage T4 DNA packaging/terminase genes 16 and 17 reveals a common ATPase center in the large subunit of viral terminases.

Mitchell MS, Matsuzaki S, Imai S, Rao VB.

Department of Biology, 103 McCort Ward Hall, The Catholic University of America, 620 Michigan Avenue, NE, Washington, DC 20064, USA.

Phage DNA packaging is believed to be driven by a rotary device coupled to an ATPase 'motor'. Recent evidence suggests that the phage DNA packaging motor is one of the strongest force-generating molecular motors reported to date. However, the ATPase center that is responsible for generating this force is unknown. In order to identify the DNA translocating ATPase, the sequences of the packaging/terminase genes of coliphages T4 and RB49 and vibriophages KVP40 and KVP20 have been analyzed. Alignment of the terminase polypeptide sequences revealed a number of functional signatures in the terminase genes 16 and 17. Most importantly, the data provide compelling evidence for an ATPase catalytic center in the N-terminal half of the large terminase subunit gp17. An analogous ATPase domain consisting of conserved functional signatures is also identified in the large terminase subunit of other bacteriophages and herpesviruses. Interestingly, the putative terminase ATPase domain exhibits some of the common features found in the ATPase domain of DEAD box helicases. Residues that would be critical for ATPase catalysis and its coupling to DNA packaging are identified. Com binatorial mutagenesis shows that the predicted threonine residues in the putative ATPase coupling motif are indeed critical for function.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235385&dopt=Abstract

Can J Microbiol. 2002 Oct;48(10):886-94.
Effect of a combination therapy between IL-12 and soluble IL-4 receptor (sIL-4R) on Candida albicans and herpes simplex virus type I infections in thermally injured mice.

Kobayashi M, Takahashi H, Herndon DN, Pollard RB, Suzuki F.

Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, USA.

The effectiveness of a combination using IL-12 and soluble IL-4 receptor (sIL-4R) to treat severe infections of herpes simplex virus type 1 (HSV-1) and Candida albicans in thermally injured mice was investigated. Although sIL-4R decreased burn-associated type 2 T-cell responses, the effect of sIL-4R was minimal on the morbidity and mortality of thermally injured mice exposed to 250 times LD50 of HSV-1 or 10 times LD50 of C. albicans. Compared with 100% mortality in control mice, mortality for HSV-1 and C. albicans was 40 and 20%, respectively, in thermally injured mice that received IL-12 and sIL-4R in combination. After stimulation with anti-CD3 monoclonal antibody, splenic T cells from thermally injured mice exposed to large amounts of HSV-1 or C. albicans did not produce gamma interferon (IFN-gamma) into their culture fluids. However, IFN-gamma was produced by splenic T cells from thermally injured and infected mice treated with IL-12 and sIL-4R in combination. These results suggest that therapeutic treatment with a combination of IL-12 and sIL-4R may be effective by inducing type 1 T-cell responses in thermally injured mice exposed to large amounts of HSV-1 or C. albicans.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12489778&dopt=Abstract

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