Helminth infections are among the neglected tropical diseases affecting billions of people globally, predominantly in developing countries. Helminths’ effects are augmented by coincident tuberculosis disease, which infects a third of the world’s population. The role of helminth infections on the pathogenesis and pathology of active tuberculosis (T.B.) remains controversial. Parasite-induced suppression of the efficacy of Bacille Calmette-Guerin (BCG) has been widely reported in helminth-endemic areas worldwide. T.B. immune response is predominantly proinflammatory T-helper type 1 (Th1)-dependent. On the other hand, helminth infections induce an opposing anti-inflammatory Th2 and Th3 immune-regulatory response. This review summarizes the literature focusing on host immune response profiles during single-helminth, T.B. and dual infections. It also aims to necessitate investigations into the complexity of immunity in helminth/T.B. coinfected patients since the research data are limited and contradictory. Helminths overlap geographically with T.B., particularly in Sub-Saharan Africa. Each disease elicits a response which may skew the immune responses. However, these effects are helminth species-dependent, where some parasites have no impact on the immune responses to concurrent T.B. The implications for the complex immunological interactions that occur during coinfection are highlighted to inform government treatment policies and encourage the development of high-efficacy T.B. vaccines in areas where helminths are prevalent.

Herpes simplex virus type 2 (HSV-2) and helminth infections are among the most widespread infectious diseases in sub-Saharan Africa (SSA). Helminths are known to modulate host immune responses and consequently impact the severity and outcomes of unrelated diseases, including allergies, autoimmune conditions, and infectious diseases. In this way, helminths may modulate essential immune responses against HSV-2 during co-infection and may alter susceptibility to and pathology of HSV-2. However, the epidemiology of STH/HSV-2 co-infections is understudied, and whether helminths influence the host immune response to HSV-2 is not well understood. In this perspective piece, we briefly examine the current knowledge on helminth immune modulation of important pathogens that are endemic to SSA, arguing that it is important to explore HSV-2 and helminth co-infections to elucidate potential interactions between HSV-2 and helminths. This is particularly relevant in SSA, where both pathogens are highly prevalent.

Introduction. Intestinal helminths and microbiota share the same anatomical niche during infection and are likely to interact either directly or indirectly. Whether intestinal helminths employ bactericidal strategies that influence their microbial environment is not completely understood. Hypothesis. In the present study, the hypothesis that the adult hookworm Nippostrongylus brasiliensis produces molecules that impair bacterial growth in vitro, is tested. Aim. To investigate the in vitro bactericidal activity of Nippostrongylus brasiliensis against commensal and pathogenic bacteria. Methodology. The bactericidal effect of somatic extract and excretory-secretory products of adult Nippostrongylus brasiliensis on Gram-positive ( Staphylococcus aureus ) and Gram-negative ( Escherichia coli , Salmonella enterica serovar Typhimurium, and Klebsiella pneumoniae ) bacteria was assessed using growth assays. Minimum inhibitory concentration and minimum bactericidal concentration assays were performed using excretory-secretory products released from the pathogen. Results. Broad-spectrum in vitro bactericidal activity in excretory-secretory products, but not somatic extract of adult Nippostrongylus brasiliensis was detected. The bactericidal activity of excretory-secretory products was concentration-dependent, maintained after heat treatment, and preserved after repeated freezing and thawing. Conclusion. The results of this study demonstrate that helminths such as Nippostrongylus brasiliensis release molecules via their excretory-secretory pathway that have broad-spectrum bactericidal activity. The mechanisms responsible for this bactericidal activity remain to be determined and further studies aimed at isolating and identifying active bactericidal molecules are needed.

Sub-Saharan Africa is heavily burdened with human immunodeficiency virus (HIV) and helminth infections, which are potent activators of pro-inflammatory and anti-inflammatory immune responses, respectively. Considering that helminths (such as Necator americanus, Ancylostoma duodenale, Ascaris lumbricoides, Trichuris trichiura, Schistosoma haematobium, and Schistosoma mansoni) can potentially dampen the production and expression of vital anti-viral pro-inflammatory cytokines, leading to enhanced HIV replication and severity, well-designed intervention studies are needed which will offer conclusive data on the nature of these interactions and the impact of deworming in HIV-infected patients. Such research will impact governmental health policies and deworming programmes, allowing for the implementation of integrated systems that will contribute to the overall improvement of African health systems.

Sub-Saharan Africa (SSA) bears a disproportionate and overlapping burden of soil-transmitted helminths (STHs) and sexually transmitted viral infections. An estimated 232 million pre-school and school-aged children in SSA are vulnerable to STH infections. Together with this, SSA has a high prevalence of herpes simplex virus type II (HSV-2), the primary cause of genital herpes. Studies have examined the immunological interactions between STHs and human immunodeficiency virus and human papillomavirus during co-infections. However, epidemiological and immunological studies on STH-HSV-2 co-infections are lacking, therefore their impact on sexual and reproductive health is not fully understood. STH-driven Th2 immune responses are known to downregulate Th1/Th17 immune responses. Therefore, during STH-HSV-2 co-infections, STH-driven immune responses may alter host immunity to HSV-2 and HSV-2 pathology. Herein, we provide an overview of the burden of STH and HSV-2 infections in SSA, and host immune responses to STH and HSV-2 infections. Further, we emphasize the relevance and urgent need for (i) focused research into the interactions between these important pathogens, and (ii) integrated approaches to improve the clinical detection and management of STH-HSV-2 co-infections in SSA.

Over the last two decades, the field of microRNA (miRNA) research has grown significantly. MiRNAs are a class of short, single-stranded, non-coding RNAs that regulate gene expression post-transcriptionally. Thereby, miRNAs regulate various essential biological processes including immunity. Dysregulated miRNAs are associated with various infectious and non-infectious diseases. Recently co-infection with soil-transmitted helminths (STHs) and herpes simplex virus type 2 (HSV-2) has become a focus of study. Both pathogens can profoundly influence host immunity, particularly in under-resourced and co-endemic regions. It is well known that STHs induce immunomodulatory responses that have bystander effects on unrelated conditions. Typically, STHs induce T-helper 2 (Th2) and immunomodulatory responses, which may dampen the proinflammatory T-helper 1 (Th1) immune responses triggered by HSV-2. However, the extent to which STH co-infection influences the host immune response to HSV-2 is not well understood. Moreover, little is known about how miRNAs shape the immune response to STH/HSV-2 co-infection. In this article, we explore the potential influence that STH co-infection may have on host immunity to HSV-2. Because STH and HSV-2 infections are widespread and disproportionately affect vulnerable and impoverished countries, it is important to consider how STHs may impact HSV-2 immunity. Specifically, we explore how miRNAs contribute to both helminth and HSV-2 infections and discuss how miRNAs may mediate STH/HSV-2 co-infections. Insight into miRNA-mediated immune responses may further improve our understanding of the potential impact of STH/HSV-2 co-infections.