HIV-1 and HIV-2 are co-endemic in certain geographic areas. HIV-2 is more weakly pathogenic than HIV-1, and progression to AIDS occurs less frequently and over a longer period of time. Recent epidemiologic studies suggest that individuals infected with HIV-2 have a lower risk of HIV-1 infection. Both immune mechanisms and various modes of viral interference have been proposed to account for these results. Our findings, described in this paper, suggest that HIV-2 inhibits HIV-1 replication. To study the molecular interactions between HIV-1 and HIV-2, proviral clones were transfected alone or in combination into the human T cell line CEM. LTR-CAT indicator constructs were included for the purpose of monitoring viral promoter activity. Viral replication in transfected cells was monitored by p24 antigen capture assay of cell culture supernatants and Western blot analysis of cell extracts. HIV-2 inhibited HIV-1 replication as determined by intracellular and extracellular p24 antigen levels. Similar results were obtained with simultaneous virus infection using HIV-1 and HIV-2, rather than transfections of proviral DNA. Using cotransfection of HIV-1 and HIV-2 LTR indicator gene constructs, the mechanism of inhibition was found to be suppression of the HIV-1 LTR by HIV-2. The inhibitory effect of HIV-2 is not due to Tat-2, but appears to discriminate between the HIV-1 and HIV-2 LTRs based on differences in the Tat activation response element, TAR. These results suggest both a molecular mechanism for HIV-2 interference with HIV-1 replication and a potential molecular approach to therapy.

Background: Ocular tumors are commonly encountered in ophthalmic practice. Objective: To study the clinical pattern of ocular tumors in the eastern region of Nepal. Materials and methods: The hospital records of patients with ocular tumors treated at B P Koirala Institute of Health Sciences in the eastern region of Nepal over a period of 5 years (April 2003 - March 2008) were studied retrospectively. Results: Of 115 consecutive patients with ocular tumors, 40 (34.75%) were below the age of 21 years, 41 (35.65%) were in the age group of 21-50 years and 34 (29.56%) of age above 50 years. There were 48 (41.73%) and 67 (58.26%) patients with benign and malignant tumors respectively. The common benign tumors were conjunctival papilloma, dermoid cysts, nevus, cystic lesions and hemangioma. Among the malignant tumors, basal cell carcinoma was the commonest (22.38%). Retinoblastoma was the most common ocular malignant tumor in the pediatric age group (88.8%). Basal cell carcinoma was the commonest eyelid malignancy 53.57%. Conclusion: Conjunctival papilloma, dermoid cysts, nevus, cystic lesions and hemangioma are common benign ocular tumors, whereas basal cell carcinoma and retinoblastoma are the commonest ocular malignancies in adults and children respectively. Key words: ocular malignancy; retinoblastoma; basal cell carcinoma DOI: 10.3126/nepjoph.v1i1.3667 Nep J Oph 2009;1(1):9-12

Several parameters of the biology of cancer of the prostate have been reviewed with a continuing assessment of the possible etiologic role of virus. These aspects include epidemiology, clinical studies, morphology, pathology, enzymology, immunology, endocrinology, model animal studies, in vitro systems, and viral investigations. From available literature it is concluded that, to date, the association with several urogenital tissues of herpes-type viruses has been best documented. It is suggested that a fundamental barrier to more sophisticated virologic and biologic studies is the lack of long term cell cultures of normal and pathologic prostate epithelium from males of all ages.

17beta-Estradiol and testosterone bind to both native and denatured DNA, and to RNA and poly(A)-poly(U). Binding affinity depends on the conformation of nucleic acid. Lowering the electrolyte concentration and raising the temperature increase the binding of 17beta-estradiol to native DNA and decrease that to denatured DNA. In 0.01 M NaCl and at 37 degrees, more 17beta-estradiol is bound to native DNA than to denatured DNA. Higher binding of steroid to denatured DNA relative to native DNA at low temperature and high ionic strength is related to larger fraction of binding sites per unit nucleotide in denatured DNA. In addition to 17beta-estradiol and testosterone, 17alpha-estradiol, 17beta-estradiol-3-methyl ether and 19-nortestosterone also stabilize the structure of nucleic acids and poly(A)-poly(U) against thermal denaturation. The 17beta-estradiol induced elevation of the T-m of DNA is diminished by methanol or high NaCl concentration. These results indicate the involvement of hydrogen bonding and hydrophobic interactions between steroids and nucleic acids. The results of binding isotherms and optical studies suggest a conformational dependence of the binding of steroids to nucleic acids.