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Jpn J Ophthalmol. 2002 Jul-Aug;46(4):370-76.
The effect of immunization with herpes simplex virus glycoprotein D fused with interleukin-2 against murine herpetic keratitis.

Inoue T, Inoue Y, Nakamura T, Yoshida A, Inoue Y, Tano Y, Shimomura Y, Fujisawa Y, Aono A, Hayashi K.

Department of Ophthalmology, Osaka University Medical School, Suita, Japan.

PURPOSE: To evaluate the preventive effect of vaccination using fusion protein (gD-IL-2) consisting of herpes simplex virus type 1 (HSV-1) glycoprotein D (gD), and human interleukin-2 (IL-2), and plasmid DNA encoding gD-IL-2 against murine herpetic keratitis. METHODS: Plasmid containing gD-IL-2 (pHDLneo1) was constructed, and gD-IL-2 peptide was purified. BALB/c mice were injected hypodermally or subconjunctivally twice with 1 microg/0.1 mL of gD-IL-2 peptide, or subconjunctivally twice with 90 microg/0.05 mL of gD-IL-2 plasmid DNA. Neutralizing antibody titer and delayed-type hypersensitivity (DTH) against HSV-1 were measured. Immunized mice were challenged with CHR3 strain of HSV-1 into the cornea. Clinical manifestations of the epithelial and stromal keratitis were scored. RESULTS: Stromal keratitis was inhibited in gD-IL-2 peptide- or DNA-immunized mice; however, epithelial keratitis was not. It was confirmed that plasmid gD-IL-2 elicited significant virus neutralizing titer in sera and DTH response. CONCLUSION: Vaccination with gD-IL-2 was effective against murine herpetic keratitis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225814&dopt=Abstract

J Neuroimmunol. 2002 Sep;130(1-2):117-27.
Infiltration of T-lymphocytes in the brain after anterior chamber inoculation of a neurovirulent and neuroinvasive strain of HSV-1.

Archin NM, Atherton SS.

Department of Microbiology, University of Texas Health Science Center at San Antonio, 78229, San Antonio, TX, USA.

Following anterior chamber (AC) inoculation of BALB/c mice with the KOS strain of herpes simplex virus type 1 (HSV-1), or with H129, a neuroinvasive and neurovirulent strain of HSV-1, both strains of virus spread from the injected eye through the brain to cause retinitis. However, KOS-infected mice develop retinitis in the uninoculated eye only, whereas H129-infected mice develop bilateral retinitis. Previous studies have shown that infiltrating T-cells in the suprachiasmatic nuclei (SCN) of the hypothalamus of KOS-infected mice concomitant with or before virus protect KOS-infected mice from ipsilateral retinitis. To determine the timing of T cell infiltration and cytokine production in the brain of H129-infected mice, adjacent, frozen sections of the brain were immunostained for virus, T-cells, IL-2, TNF-alpha or IFN-gamma. T-cells infiltrated the brains of H129-infected mice and cytokines were produced in infected tissues. However, virus spread to the optic nerve and retina of both the inoculated and uninoculated eye before T-cells and cytokines were detected in the SCN of H129-infected mice. These results suggest that infiltrating T-cells in the SCN of H129-infected mice may arrive too late to prevent the spread of virus into the optic nerves and retinas and thus prevent development of bilateral retinitis in infected mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225894&dopt=Abstract

J Med Virol. 2002 Nov;68(3):378-83.
Epstein-Barr virus (types 1 and 2) in the tear film in Sjogren's syndrome and HIV infection.

Willoughby CE, Baker K, Kaye SB, Carey P, O'Donnell N, Field A, Longman L, Bucknall R, Hart CA.

St. Paul's Eye Unit, Royal Liverpool University Hospital, Liverpool, United Kingdom.

Evidence of Epstein-Barr virus (EBV) shedding in the saliva and tear film has been sought to explain the pathogenesis of the oral and ocular features of Sjogren's syndrome. Patients with human immunodeficiency virus (HIV) infection are purported to have a higher incidence of keratoconjunctivitis sicca. Twenty patients with definite Sjogren's syndrome (primary and secondary), 19 with HIV infection, and 15 normal controls were recruited and studied. Human herpes viruses (EBV 1 and 2, CMV, HZV, and HSV-1) in tear film were detected by polymerase chain reaction of DNA extracted from Schirmer strips. HSV-1, VZV, and CMV were not detected in any tear samples. EBV-1 DNA was found in the tear film of 4 patients with Sjogren's syndrome, which was not significantly different from the control group (P = 0.18). Twelve patients with HIV infection had evidence of EBV-1 in their tears, which was significantly different from controls (P = 0.0002) and patients with Sjogren's syndrome (P = 0.014). EBV-2 was found in 3 patients with HIV and in 1 patient with secondary Sjogren's syndrome, and was always found as a co-infection with EBV-1 (P = 0.01). This represents the first report examining EBV types 1 and 2 in the tear film and also EBV in the tear film of patients with HIV. Shedding of EBV in the tear film was not related to the presence of keratoconjunctivitis sicca in Sjogren's syndrome. EBV-2 co-infection with EBV-1 has not been previously reported in the tear film. EBV infection is abnormally regulated in Sjogren's syndrome and HIV, and it is likely that the presence of EBV in the tear film is related to the patients' altered immune status. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226825&dopt=Abstract

J Med Virol. 2002 Nov;68(3):399-403.
Quantification of human herpesvirus 8 by real-time PCR in blood fractions of AIDS patients with Kaposi's sarcoma and multicentric Castleman's disease.

Boivin G, Cote S, Cloutier N, Abed Y, Maguigad M, Routy JP.

Centre Hospitalier Universitaire de Quebec (CHUQ-CHUL) and Laval University, Quebec City, Canada. guy.boivichul.ulaval.ca

Few studies have assessed human herpesvirus 8 (HHV8) viremia levels in different HHV8-related pathologies, using sensitive and reproducible molecular assays. Our objective was to compare the HHV8 DNA load in serial blood samples (collected every 3 months for 1 year) from acquired immunodeficiency syndrome (AIDS) patients with Kaposi's sarcoma (KS) and multicentric Castleman's disease (MCD). The HHV8 viral load was determined in both peripheral blood mononuclear cells (PBMC) and plasma fractions, using a competitive real-time polymerase chain reaction (PCR) assay developed in a LightCycler instrument (Roche Diagnostics). In six subjects with limited or extensive KS while on highly active antiretroviral therapy, the HHV8 DNA load was either undetectable (<50 copies/10(5) cells) or low (</=135 copies) in all PBMC samples. In contrast, the cellular HHV8 load was >1,000 copies in at least one of the samples from the two subjects with both KS and MCD. HHV8 DNA was detected in plasma only when the cellular viral load was >10,000 copies/10(5) cells. After chemotherapy, the HHV8 DNA load became undetectable in the MCD patients despite no changes in CD4 T-cell counts or highly active antiretroviral therapy (HAART) regimens. These results suggest that the pathogenesis of the two HHV8-associated diseases (i.e., KS and MCD) might be different, as only the latter was associated with important viremia in our patients. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226828&dopt=Abstract

J Med Virol. 2002 Nov;68(3):404-11.
Human interleukin-6 induces human herpesvirus-8 replication in a body cavity-based lymphoma cell line.

Song J, Ohkura T, Sugimoto M, Mori Y, Inagi R, Yamanishi K, Yoshizaki K, Nishimoto N.

Department of Medical Science I, School of Health and Sport Sciences, Osaka University, Osaka, Japan.

Human herpesvirus-8 (HHV-8) is etiologically associated with Kaposi's sarcoma (KS), body cavity-based lymphoma (BCBL), and multicentric Castleman's disease (MCD). These HHV-8-associated diseases arise predominantly in acquired immunodeficiency syndrome (AIDS) patients. Human interleukin-6 (huIL-6) elevated in the serum of AIDS patients is suggested to stimulate the growth of KS and BCBL and to augment the symptoms of MCD. To determine whether huIL-6 stimulates HHV-8 replication directly, expression of the HHV-8 ORF-50 immediate-early gene (transcription activator) and ORF-26 late lytic gene (a capsid protein) was assessed in a BCBL-1 cell line stimulated by huIL-6 by means of real-time reverse transcription-polymerase chain reaction. huIL-6 induced both ORF-50 and ORF-26 expression, and the maximal ORF-50 expression appeared earlier than that of ORF-26. The data indicate that huIL-6 reactivates HHV-8 in BCBL-1 cells through inducing ORF-50. We also confirmed the previously reported activities of HHV-8-encoded huIL-6 homologue (viral interleukin-6 [vIL-6]) on human immunodeficiency virus (HIV) replication in U1 cell line and huIL-6 production by MT-4 T cells, and utilizing monoclonal antibodies to the huIL-6 receptor components, we elucidated that gp130 is the signaling molecule necessary for these vIL-6 activities. These data suggest the possible existence of interaction between HIV and HHV-8 via IL-6, and that the blockade of IL-6 signal by anti-IL-6R antibody or anti-gp130 antibody can constitute a strategy to treat HIV/HHV-8 dually infected patients. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226829&dopt=Abstract

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