BackgroundSilver nanoparticles have proven to exert antiviral activity against HIV-1 at non-cytotoxic concentrations, but the mechanism underlying their HIV-inhibitory activity has not been not fully elucidated. In this study, silver nanoparticles are evaluated to elucidate their mode of antiviral action against HIV-1 using a panel of different in vitro assays.ResultsOur data suggest that silver nanoparticles exert anti-HIV activity at an early stage of viral replication, most likely as a virucidal agent or as an inhibitor of viral entry. Silver nanoparticles bind to gp120 in a manner that prevents CD4-dependent virion binding, fusion, and infectivity, acting as an effective virucidal agent against cell-free virus (laboratory strains, clinical isolates, T and M tropic strains, and resistant strains) and cell-associated virus. Besides, silver nanoparticles inhibit post-entry stages of the HIV-1 life cycle.ConclusionsThese properties make them a broad-spectrum agent not prone to inducing resistance that could be used preventively against a wide variety of circulating HIV-1 strains.

Bacterial pathogens are known to pester Mankind from times immemorial; even though significant efforts in getting rid of these harmful microbes have been made the results are very faint with only few organisms that have been eradicated, such as Small pox virus. But the efforts to eradicate bacterial diseases have shown no passable results as in case of viruses. This is due to the exceptional adaptation and transformation abilities of bacteria to varying environmental Conditions. Though a large number of antibiotics are being used from decades now, there are no affirmative solutions available due to resistance developed towards antibiotics by these bacteria. This resistance developed by the bacteria calls for dire necessity to discover new drugs which can at least reduce the hazards posed by these microbes if not eradication. Hence in this study we have focused on bio prospecting of Clerodendrum paniculatum and Saraca asoka against the highly virulent and extremely adaptable organisms E. coli and K. pneumoniae which currently pose a severe threat to humans due to their acquired resistance to large number of antibiotics.

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Zika virus (ZIKV) invades and persists in the central nervous system (CNS), causing severe neurological diseases. However the virus journey, from the bloodstream to tissues through a mature endothelium, remains unclear. Here, we show that ZIKV-infected monocytes represent suitable carriers for viral dissemination to the CNS using human primary monocytes, cerebral organoids derived from embryonic stem cells, organotypic mouse cerebellar slices, a xenotypic human-zebrafish model, and human fetus brain samples. We find that ZIKV-exposed monocytes exhibit higher expression of adhesion molecules, and higher abilities to attach onto the vessel wall and transmigrate across endothelia. This phenotype is associated to enhanced monocyte-mediated ZIKV dissemination to neural cells. Together, our data show that ZIKV manipulates the monocyte adhesive properties and enhances monocyte transmigration and viral dissemination to neural cells. Monocyte transmigration may represent an important mechanism required for viral tissue invasion and persistence that could be specifically targeted for therapeutic intervention.