People living with human immunodeficiency virus (HIV) demonstrate highly expressed immune deficiency and are vulnerable to exogenous viral infections (co-infections), including influenza. We were interested in developing an in vitro model to examine HIV-1 and influenza virus (Flu) co-infection based on HIV-1 sialoglycoprotein (Sgp) synthesis and virus replication in double-infected cells. A convenient and reproducible experimental model for studying the sialylation of HIV-1 glycoprotein 120 (Gp120) by direct radioactive precursors of sialic acid synthesis, [¹⁴C]N-acetylmannosamine) in cell culture was successfully introduced for investigation of co-infection. The co-infection provoked desialylation of viral Sgps, followed initially by decreased and later on, by increased HIV replication. Monoclonal antibodies (Mab) to the main Gp120 V3 neutralization epitope but not to broadly reactive Mab against Gp120 recognize and neutralize the newly exposed epitopes. A hypothesis was outlined that exogenous neuraminidase (NA) (Flu virus) changes the configuration of HIV-1 Gp120 through desialylation resulting in the exposure of a novel antigen. The proposed model could contribute to better understanding of pathogenesis of Flu co-infection in people living with HIV. In vivo, Flu co-infection most probably leads to desialylation of both HIV and the cell surface, thus facilitating the escape of HIV from immune control. The findings described here reflect the interaction between components of two viruses – NA of Flu virus and Sgps on HIV-1 surface without considering the cell surface. The hypothesis could be extended to other exogenous co-infections with agents containing NA in HIV-infected people.

Recently, essential rose oils and rose products have gained increasing importance in both the cosmetic and food industries, as well as in the composition of medicinal products. We investigated the in vitro antiviral activity of essential oil and floral water from Rosa damascena Mill against herpes simplex virus type 1 (HSV-1) infection in rabbit retinal cells (RRCs). The composition of the main chemical components in the rose essential oil was determined by means of gas chromatographic analysis. The effect on the viral replication cycle was determined using the cytopathic effect (CPE) inhibition assay. The virucidal activity, the effect on the adsorption stage of the virus to the host cell, and the protective effect on healthy cells were evaluated using the endpoint dilution method. The effects were determined as deviation in the viral titer, Δlg, for the treated cells from the one for the untreated viral control. The identified main active components of rose oil are geraniol (28.73%), citronellol (21.50%), nonadecane (13.13%), nerol (5.51%), heneicosane (4.87%), nonadecene (3.93), heptadecane (2.29), farnesol (2.11%), tricosane (1.29%), eicosane (1.01%), and eugenol (0.85%). The results demonstrated that both rose products do not have a significant effect on the virus replication but directly affect the viral particles and reduce the viral titer by Δlg = 3.25 for floral water and by Δlg = 3.0 for essential oil. Significant inhibition of the viral adsorption stage was also observed, leading to a decrease in the viral titers by Δlg = 2.25 for floral water and by Δlg = 2.0 for essential oil. When pretreating healthy cells with rose products, both samples significantly protected them from subsequent infection with HSV-1. This protective effect was more pronounced for the oil (Δlg = 2.5) compared to the one for the floral water (Δlg = 2.0). We used the in silico molecular docking method to gain insight into the mechanism of hindrance of viral adsorption by the main rose oil compounds (geraniol, citronellol, nerol). These components targeted the HSV-1 gD interaction surface with nectin-1 and HVEM (Herpesvirus Entry Mediator) host cell receptors, at N-, C-ends, and N-end, respectively. These findings could provide a structural framework for further development of anti-HSV-1 therapeutics.

The side effects of conventional cancer treatments, such as chemotherapy, radiotherapy, etc., worsen the quality of life of patients. Therefore, it is necessary to explore the possibilities of creating new drugs containing natural products with low toxicity. The experimental scientific pharmacological research of rose preparations in Bulgaria began in the first half of the 20th century. Bulgarian rose essential oil (BREO) is qualified by GC FID analysis. To study the effect of the BREO, we used HCT-8 and HT-29 tumor cell lines. As a model of healthy tissue, we used the non-tumorigenic cells MCF-12F. Cells were treated with twofold increasing concentrations of BREO from 7.5 µg/mL to 1000 µg/mL. The NRU test and MTT assay were used for evaluation of the safety, antiproliferative activity and colony formation assay. Our results showed low cytotoxicity (CC₅₀ = 629.72 ± 22.38 μg/mL) and high level of photosafety (PIF = 0.92) of BREO. The antiproliferative activity test shows that the BREO has an IC₅₀ = 290.45 ± 10.79 μg/mL for the HT-29 cells. In the normal cell line MCF-12F, this effect is lower (IC₅₀ = 383.90 ± 34.75 μg/mL). Furthermore, colony forming assay showed a significant reduction in IC₅₀ value (IC₅₀ = 163.79 ± 10.25 μg/mL) in HT-29 cells. The in silico experiments confirmed the potential of the BREO for antiproliferative effect and further activation of different pathways leading to apoptosis.

Sialyltransferases (ST) are a family of enzymes specifically transporting sialic acids (SAs) onto nascent glycoproteins and glycolipids, so participating in glycoprotein synthesis. The envelope of human immunodeficiency virus—type 1 (HIV-1) is highly glycosylated and sialylated. Here we report for the first time data on ST-activity in acutely and chronically HIV-1 infected cells in cell culture. The results demonstrated higher ST activity in cytosols of both acutely and chronically infected cells compared to uninfected ones. Data fit well to our earlier assumption about the virus specific character of sialylation, found by using of direct radioactive precursor of biosynthesis of SAs as terminal moieties of sialoglycopro-teins (Sgps) of HIV-1 in cell culture.