The COVID-19, tuberculosis and HIV/AIDS: Ménage à Trois

In December 2019, a novel pneumonic condition, Coronavirus disease 2019 (COVID- 19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), broke out in China and spread globally. The presentation of COVID-19 is more severe in persons with underlying medical conditions such as Tuberculosis (TB), Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS) and other pneumonic conditions. All three diseases are of global concern and can significantly affect the lungs with characteristic cytokine storm, immunosuppression, and respiratory failure. Co-infections of SARS-CoV-2 with HIV and Mycobacterium tuberculosis (Mtb) have been reported, which may influence their pathogenesis and disease progression. Pulmonary TB and HIV/AIDS patients could be more susceptible to SARS-CoV-2 infection leading to lethal synergy and disease severity. Therefore, the biological and epidemiological interactions of COVID-19, HIV/AIDS, and TB need to be understood holistically. While data is needed to predict the impact of the COVID-19 pandemic on these existing diseases, it is necessary to review the implications of the evolving COVID-19 management on HIV/AIDS and TB control, including therapy and funding. Also, the impact of long COVID on patients, who may have this co-infection. Thus, this review highlights the implications of COVID-19, HIV/AIDS, and TB co-infection compares disease mechanisms, addresses growing concerns, and suggests a direction for improved diagnosis and general management

Pathogen-Induced Epigenetic Modifications in Cancers: Implications for Prevention, Detection and Treatment of Cancers in Africa

Cancer is a major public health burden worldwide. Tumor formation is caused by multiple intrinsic and extrinsic factors. Many reports have demonstrated a positive correlation between the burden of infectious pathogens and the occurrence of cancers. However, the mechanistic link between pathogens and cancer development remains largely unclear and is subject to active investigations. Apart from somatic mutations that have been widely linked with various cancers, an appreciable body of knowledge points to alterations of host epigenetic patterns as key triggers for cancer development. Several studies have associated various infectious pathogens with epigenetic modifications. It is therefore plausible to assume that pathogens induce carcinogenesis via alteration of normal host epigenetic patterns. Thus, Africa with its disproportionate burden of infectious pathogens is threatened by a dramatic increase in pathogen-mediated cancers. To curb the potential upsurge of such cancers, a better understanding of the role of tropical pathogens in cancer epigenetics could substantially provide resources to improve cancer management among Africans. Therefore, this review discusses cancer epigenetic studies in Africa and the link between tropical pathogens and cancer burden. In addition, we discuss the potential mechanisms by which pathogens induce cancers and the opportunities and challenges of tropical pathogen-induced epigenetic changes for cancer prevention, detection and management

Electrochemical evaluation of ion substituted-hydroxyapatite on HeLa cells plasma membrane potential

This study reports the electrochemical activities of a novel ion substituted-Hydroxyapatite (HAp) material in contact with HeLa cells. The work was performed to evaluate the inhibitory effects of various concentrations of HAp on ion transfer mechanisms in HeLa cells. The materials (n = 2: HAp1 and HAp3) were prepared at different stirring times from Achatina achatina snail shells and phosphate-containing solution. The structure of the materials and the trace elements concentration were evaluated using x-ray diffractometry and infrared spectrometry as well as atomic absorption spectroscopy. Electrochemical studies conducted on the cells after 30 min of exposure to the materials demonstrated different responses as elucidated by cyclic voltammetry. The voltammograms revealed HAp1 to be non-redox whereas HAp3 was redox active. Minimal concentrations of HAp1 showed high anodic peak current when compared to the HeLa cells alone, indicating a hyperpolarization of the cells. The peak current gradually reduced as the concentration of HAp1 was increased, and then followed by a sudden rise suggesting inhibition of the cell action potential. HAp3 showed a wavy pattern of the anodic peak current when the material concentration was varied. Peak currents of $$0.92 \pm 0.03$$ nA and $$0.57 \pm 0.01$$ nA were recorded for HAp1 and HAp3, respectively at the highest concentration of 5 µL. The results suggest that different inhibitory mechanisms are at play on the voltage-gated ion channels of the cells, indicating the possibility of using the materials to achieve different cancer proliferation inhibition

Chitosan-Coated Halloysite Nanotubes As Vehicle for Controlled Drug Delivery to MCF-7 Cancer Cells In Vitro

The aim of the work is to improve the release properties of curcumin onto human breast cancer cell lines using coated halloysite nanotubes (HNTs) with chitosan as a polycation. A loading efficiency of 70.2% (w/w) was attained for loading 4.9 mg of the drug into 0.204 g bed volume of HNTs using the vacuum suction method. Results acquired from Brunauer-Emmett-Teller (BET), Fourier-transform infrared (FTIR) spectroscopy, transmission electron microscopy (TEM), scanning electron spectroscopy (SEM), zeta potential, and thermogravimetric analysis (TGA) indicated the presence of the drug and the biopolymer in and around the nanotubes. The release properties of drug-loaded HNTs (DLHNTs) and chitosan-coated drug-loaded HNTs (DLHNTs-CH) were evaluated. The release percentages of DLHNTs and DLHNTs-CH after 6 h were 50.7 and 37%, respectively. Based on the correlation coefficients obtained by fitting the release nature of curcumin from the two samples, the Korsmeyer-Peppas model was found to be the best-fitted model. In vitro cell viability studies were carried out on the human breast cancer cell line MCF-7, using the MTT and trypan blue exclusion assays. Prior to the Trypan blue assay, the IC50 of curcumin was determined to be ~30 µM. After 24 h of incubation, the recorded cell viability values were 94, 68, 57, and 51% for HNTs, DLHNTs-CH, DLHNTs, and curcumin, respectively. In comparison to the release studies, it could be deducted that sustained lethal doses of curcumin were released from the DLHNTs-CH within the same time. It is concluded from this work that the “burst release” of naked drugs could be slowly administered using chitosan-coated HNTs as potential drug carriers

Upper airway epithelial tissue transcriptome analysis reveals immune signatures associated with COVID-19 severity in Ghanaians.

The immunological signatures driving the severity of coronavirus disease 19 (COVID-19) in Ghanaians remain poorly understood. We performed bulk transcriptome sequencing of nasopharyngeal samples from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)-infected Ghanaians with mild and severe COVID-19, as well as healthy controls to characterize immune signatures at the primary SARS-CoV-2 infection site and identify drivers of disease severity. Generally, a heightened antiviral response was observed in SARS-CoV-2-infected Ghanaians compared with uninfected controls. COVID-19 severity was associated with immune suppression, overexpression of proinflammatory cytokines, including CRNN, IL1A, S100A7, and IL23A, and activation of pathways involved in keratinocyte proliferation. SAMD9L was among the differentially regulated interferon-stimulated genes in our mild and severe disease cohorts, suggesting that it may play a critical role in SARS-CoV-2 pathogenesis. By comparing our data with a publicly available dataset from a non-African (Indians) (GSE166530), an elevated expression of antiviral response-related genes was noted in COVID-19-infected Ghanaians. Overall, the study describes immune signatures driving COVID-19 severity in Ghanaians and identifies immune drivers that could serve as potential prognostic markers for future outbreaks or pandemics. It further provides important preliminary evidence suggesting differences in antiviral response at the upper respiratory interface in sub-Saharan Africans (Ghanaians) and non-Africans, which could be contributing to the differences in disease outcomes. Further studies using larger datasets from different populations will expand on these findings