The majority of new HIV infections occur in women as a result of heterosexual intercourse, overcoming multiple innate barriers to infection within the mucosa. However, the avenues through which infection is established, and the nature of bottlenecks to transmission, have been the source of considerable investigation and contention. Using a high dose of a single round non-replicating SIV-based vector containing a novel dual reporter system, we determined the sites of infection by the inoculum using the rhesus macaque vaginal transmission model. Here we show that the entire female reproductive tract (FRT), including the vagina, ecto- and endocervix, along with ovaries and local draining lymph nodes can contain transduced cells only 48 hours after inoculation. The distribution of infection shows that virions quickly disseminate after exposure and can access target cells throughout the FRT, with an apparent preference for infection in squamous vaginal and ectocervical mucosa. JRFL enveloped virions infect diverse CD4 expressing cell types, with T cells resident throughout the FRT representing the primary target. These findings establish a new perspective that the entire FRT is susceptible and virus can reach as far as the ovary and local draining lymph nodes. Based on these findings, it is essential that protective mechanisms for prevention of HIV acquisition must be present at protective levels throughout the entire FRT to provide complete protection.

Background: Hepatitis C virus (HCV) encodes two transmembrane glycoproteins E1 and E2 which form a heterodimer. E1 is believed to mediate fusion while E2 has been shown to bind cellular receptors including CD81. In this study, alanine substitutions in E2 were generated within putative CD81 binding regions to define residues critical for viral entry. The effect of each mutation was tested by challenging susceptible cell lines with mutant HCV E1E2 pseudotyped viruses generated using a lentiviral system (HCVpp). In addition to assaying infectivity, producer cell expression and HCVpp incorporation of HCV E1 and E2 proteins, CD81 binding profiles, and E1E2 association of mutants were examined.

Phytochemical study of the aqueous extract of the flowering tops of Lamium album led to identification of the antiviral iridoid isomers lamiridosins A and B (1, 2). These compounds were found to significantly inhibit hepatitis C virus entry (IC(50) 2.31 muM) in vitro. Studies of 14 iridoid analogues showed that, while the parent iridoid glucosides demonstrated no anti-HCV entry activity, the aglycones of shanzhiside methyl ester (4), loganin (5), loganic acid (6), geniposide (10), verbenalin (12), eurostoside (15), and picroside II (17) exhibited significant anti-HCV entry and anti-infectivity activities.

We identified a previously unknown neurogenic region at the dorsal surface of the hippocampus; (the “subhippocampal zone,” SHZ) in the adult brain. Using a reporter mouse in which SHZ cells and their progeny could be traced through the expression of EGFP under the control of the CXCR4 chemokine receptor promoter we observed the presence of a pool of EGFP expressing cells migrating in direction of the dentate gyrus (DG), which is maintained throughout adulthood. This population appeared to originate from the SHZ where cells entered a caudal migratory stream (aCMS) that included the fimbria, the meninges and the DG. Deletion of CXCR4 from neural stem cells (NSCs) or neuroinflammation resulted in the appearance of neurons in the DG, which were the result of migration of NSCs from the SHZ. Some of these neurons were ectopically placed. Our observations indicate that the SHZ is a neurogenic zone in the adult brain through migration of NSCs in the aCMS. Regulation of CXCR4 signaling in these cells may be involved in repair of the DG and may also give rise to ectopic granule cells in the DG in the context of neuropathology.

In this study, we measured the effects of three commonly used insecticides classified as insect growth regulators, on the encyrtid parasitoid Leptomastix dactylopii (Howard) when parasitizing citrus mealybug, Planococcus citri (Risso). Kinoprene, pyriproxyfen, and azadirachtin were evaluated in both petri dish and a cage experiment at label-recommended rates to measure their effects on the mortality, parasitization rate, and sex ratio of L. dactylopii. Insecticides were applied to petri dishes and plants either immediately before, 24 h before, or 48 h before release of the parasitoid. Kinoprene applied 24 h before parasitoid release caused 100% mortality of L. dactylopii in petri dishes within 48 h. Mortality rates for L. dactylopii exposed to azadirachtin and pyriproxyfen did not exceed 5% regardless of release time. There were no release time x insecticide interactions on L. dactylopii parasitization rate. The insecticide alone, however, did significantly affect parasitization rates of L. dactylopii on P. citri; the kinoprene treatment significantly reduced L. dactylopii parasitization rates compared with azadirachtin and pyriproxyfen. In a cage experiment with coleus, Solenostemon scutellaroides (L.) Codd, applications of both pyriproxyfen and kinoprene resulted in fewer P. citri parasitized by L. dactylopii than azadirachtin or the control. The sex ratio was equivalent in the petri dish experiment, whereas in the cage experiment the sex ratio was biased toward males, particularly for the kinoprene treatment. Based on the results from this study, we suggest that kinoprene is not compatible with releases of L. dactylopii to control citrus mealybugs.