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Vet Immunol Immunopathol. 2002 Oct 8;89(1-2):29-36.
Effects of phenoxyethanol on the innate immune system of gilthead seabream (Sparus aurata L.) exposed to crowding stress.

Ortuno J, Esteban MA, Meseguer J.

Department of Cell Biology, Faculty of Biology, University of Murcia, 30100 Murcia, Spain.

Phenoxyethanol is routinely used in seabream aquaculture to minimise fish stress response despite the secondary negative effects which have been observed. In this study, two different doses (60 and 200 microl/l) of phenoxyethanol, sedative and narcotic, were tested for their ability to reduce the stress caused in gilthead seabream (Sparus aurata L.) by crowding. Blood glucose and serum cortisol concentrations were measured as stress indicators. In order to study the effects of the treatment on the innate immune system of crowded specimens, two parameters of the innate immune response, serum complement activity and phagocytosis, were assessed. The results show that anaesthesia itself produced a stress response in the fish and affected the immune system, although the effects were greater with the narcotic dose. When the effects of anaesthesia on crowded fish were analysed, the results pointed to a slight reduction in stress as a result of the sedative dose of phenoxyethanol (lower increase in cortisol and lower reduction in phagocytosis). However, additive negative effects were seen in crowded fish when the narcotic dose of phenoxyethanol was used. Since the use of phenoxyethanol is a common practice in aquaculture, the significance of the results should be considered.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208048&dopt=Abstract

Gynecol Oncol. 2002 Dec;87(3):268-73.
Human papillomavirus type 16 E6 and E7 gene variations in Indian cervical cancer.

Radhakrishna Pillai M, Sreevidya S, Pollock BH, Jayaprakash PG, Herman B.

Division of Laboratory Medicine, Regional Cancer Centre, Thiruvananthapuram, India. mrpillasnl.com

OBJECTIVES: Human papillomavirus type 16 is a causative factor for development of cervical cancer. The E6 and E7 genes of HPV 16 are critical to the process of immortalization and transformation of host cells. Recent reports suggest that variants of these two genes may contribute to the risk of malignant progression of cancer in the uterine cervix. However, no data exist on sequence variations of HPV 16 E6 and E7 genes that may exist in India. Therefore, we examined intratype variations in the E6 and E7 viral genes in DNA isolated from HPV 16-positive cervical scrapes and biopsies. METHODS: The open reading frames of the E6 and E7 genes were amplified by PCR and then directly sequenced by the fluorescent dye dideoxy termination method.Results. In addition to the prototype E6 gene sequence, five sets of mutations of the E6 gene were identified. The European prototype (350T) was detected in 9.1% of the study group while the European variant (350G) was seen in 28% of patients. The remaining variants (a combination of the 350G mutation with 335T, 145T, or 419G) were significantly associated with cases compared to controls. The 350G + 145T variant was found at much higher incidence in cases in younger women, suggesting that this variant may be associated with aggressive tumor behavior. Interestingly the 350G + 419G combination was found only in controls. There was no significant association between the four genotypes of E7 and any stage of tumor progression or age. CONCLUSIONS: The results indicate that specific mutations in the E6 gene are found in young Indian women with high-grade squamous intraepithelial lesions and invasive cancer, suggesting that these mutations represent more oncogenically active HPV 16. Whether this increased oncogenecity is due to differences in p53 inactivation, ineffective keratinocyte differentiation, and/or altered response to the immune system by these oncogenic E6 mutants remains to be clarified.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12468324&dopt=Abstract

J Virol. 2002 Oct;76(19):9716-23.
The adenovirus E3 RID complex protects some cultured human T and B lymphocytes from Fas-induced apoptosis.

McNees AL, Garnett CT, Gooding LR.

Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

Human group C adenoviruses cause an acute infection in respiratory epithelia and establish a long-term or persistent infection, possibly in lymphocytes. The mechanism by which this persistence is maintained is unknown; however, it would require that persistently infected lymphocytes not be deleted. The adenovirus genome encodes proteins that prevent the immune system from eliminating the virus-infected cell, including the E3 receptor internalization and degradation (RID) complex. The RID complex prevents death of infected cells by blocking apoptosis initiated through death domain-containing receptors of the tumor necrosis factor receptor (TNFR) superfamily, including TNFR1 (L. R. Gooding, T. S. Ranheim, A. E. Tollefson, L. Aquino, P. Duerksen-Hughes, T. M. Horton, and W. S. Wold, J. Virol. 65:4114-4123, 1991), TNF-related apoptosis-inducing ligand receptors (TRAIL-R1 and -R2) (C. A. Benedict, P. S. Norris, T. I. Prigozy, J. L. Bodmer, J. A. Mahr, C. T. Garnett, F. Martinon, J. Tschopp, L. R. Gooding, and C. F. Ware, J. Biol. Chem. 276:3270-3278, 2001; A. E. Tollefson, K. Toth, K. Doronin, M. Kuppuswamy, O. A. Doronina, D. L. Lichtenstein, T. W. Hermiston, C. A. Smith, and W. S. Wold, J. Virol. 75:8875-8887, 2001), and Fas (J. Shisler, C. Yang, B. Walter, C. F. Ware, and L. R. Gooding, J. Virol. 71:8299-8306, 1997). Here, we test the ability of RID to protect human lymphocytes from apoptosis induced by ligation of Fas, a mechanism important for regulating lymphocyte populations. Using a retrovirus expressing RID to infect six human lymphocyte cell lines, we found that RID functions in the absence of other viral proteins to downregulate surface Fas on some, but not all, cell lines. Total cellular levels of Fas decrease as measured by Western blotting, and this loss of Fas correlates with protection from apoptosis induced by ligation of Fas in every cell line tested. Although in some cases, RID causes loss of only a fraction of surface Fas, the presence of RID completely blocks the immediate events downstream of Fas ligation (i.e., Fas-FADD association and caspase-8 cleavage) in susceptible cell lines. Nonetheless, the ability of RID to block Fas signaling is independent of the Fas signaling pathway used (type I or type II). Interestingly, among the four T-cell lines tested, RID caused loss of Fas in the two T-cell lines bearing a relatively immature phenotype, while having no activity in T cells with mature phenotypes. Collectively, these data suggest that RID functions to prevent apoptosis of some human lymphocytes by internalizing surface Fas receptors. It is possible that the expression of RID facilitates long-term infection by preventing Fas-mediated deletion of persistently infected lymphocytes.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208950&dopt=Abstract

J Virol. 2002 Oct;76(19):10044-9.
Immune responses to the major capsid protein during parvovirus infection of rats.

Ball-Goodrich LJ, Paturzo FX, Johnson EA, Steger K, Jacoby RO.

Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8016, USA. lisa.ball-goodricale.edu

Rat virus (RV) is a common parvovirus of laboratory rodents which can disrupt rat-based research. Prenatal or perinatal infection can be pathogenic or lead to persistent infection, whereas infection of adult rats is typically self-limiting. Effects on the host immune system have been documented during RV infection, but little is known about immune responses necessary for viral clearance. Our studies were conducted to identify humoral and cellular responses to the predominant capsid protein, VP2, during experimental infection of adult rats. We observed VP2-specific proliferation, gamma interferon production, and an immunoglobulin G2a humoral response that is maintained for at least 35 days following RV infection. These results strongly suggest the induction of virus-specific Th1-mediated immunity.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208983&dopt=Abstract

J Virol. 2002 Oct;76(19):10079-83.
Association of plasma viral RNA load with prognosis in cats naturally infected with feline immunodeficiency virus.

Goto Y, Nishimura Y, Baba K, Mizuno T, Endo Y, Masuda K, Ohno K, Tsujimoto H.

Department of Veterinary Internal Medicine, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.

We measured the quantity of plasma feline immunodeficiency virus (FIV) RNA using a real-time sequence detecting system. Plasma viral RNA load was shown to correlate with the clinical stage, survival time, and disease progression in naturally FIV-infected cats. The present study indicates that the plasma viral RNA load can be used as a clinical marker representing the impairment of the immune system and predicting the clinical outcome in FIV-infected cats.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12208990&dopt=Abstract

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