Cryptosporidiosis is an intestinal disease that affects a variety of hosts including animals and humans. Since no vaccines exist against the disease till date, drug treatment is the mainstay of disease control. Nitazoxanide (NTZ) is the only FDA-approved drug for the treatment of human cryptosporidiosis. However, its efficacy in immunocompromised people such as those with AIDS, in malnourished children, or those with concomitant cryptosporidiosis is limited. In the absence of effective drugs against cryptosporidiosis, improving the efficacy of existing drugs may offer an attractive alternative. In the present work, we have assessed the potential of the cell-penetrating peptide (CPP) octaarginine (R8) to increase the uptake of NTZ. Octaarginine (R8) was synthetically attached to NTZ in an enzymatically releasable manner and used to inhibit growth of Cryptosporidium parvum in an in vitro culture system using human ileocecal adenocarcinoma (HCT-8) cell line. We observed a significant concentration-dependent increase in drug efficacy. We conclude that coupling of octaarginine to NTZ is beneficial for drug activity and it represents an attractive strategy to widen the repertoire of anti-cryptosporidial therapeutics. Further investigations such as in vivo studies with the conjugate drug will help to further characterize this strategy for the treatment of cryptosporidiosis.

The global malaria morbidity and mortality witnessed an increase from 2019 to 2020 partly due to disruptions in control programs’ activities imposed by the COVID‐19 pandemic. Therefore, there is still a significant burden of malaria in Cameroon which needs attention from all fronts to attain elimination goals. It is normally expected that a typical forest ecology that has undergone urbanization and subjected to high rates of ecological instabilities should also have a shift from characteristic perennial malaria transmission and a shift in the type of malaria endemicity plaguing such distorted forest ecology. In this observational comparative study, we randomly enrolled participants from rural and urban settings of a forest zone during a low malaria transmission period, which coincided with the onset of COVID‐19 pandemic. An optimized structured questionnaire was employed, to collect socio‐demographic data and associated risk factors. The CareStart™ Malaria HRP2 antigen test was performed on participants from both settings to determine the prevalence of community asymptomatic malaria. Of 307 participants, 188 (61.0%) were from the rural, while 119 (38.8%) from the urban community. The overall prevalence of asymptomatic malaria (27.0%) detected Plasmodium falciparum antigen in 83 participants. The urban community’s prevalence was 4.2% (5 positives) while the rural community’s was 41.5% (78 positives). In simple logistic regression models, rural forest community and farm around the house were statistically significant predictors of testing positive (coefficient 2.8, 95% CI 1.8‐3.7, p value<0.001) and (coefficient 3.1, 95% CI 1.1‐5.1, p value =0.003), respectively. In the multivariate model, the strongest predictor of testing positive was living in a rural community, with p < 0.001 and odds ratio of 10.9 (95% CI, 3.8‐31.8). These results indicate that during a low transmission period, the prevalence of asymptomatic malaria differs between depleted urban and rural forested settings, suggesting a need for strategic target intervention for the control of asymptomatic malaria.

Cryptosporidiosis remains a major cause of diarrhea-related childhood death, particularly in developing countries. Although effective anti-retroviral therapy has significantly reduced the cryptosporidiosis burden in western nations, the situation in developing countries remains alarming due to limited therapeutic options and a lack of preventive measures. To better control disease transmission and develop effective prevention strategies, a thorough understanding of the genetic diversity of circulating species is crucial. While cryptosporidiosis has previously been reported in Cameroon, information on the genetic diversity of parasite strains is lacking. In a large cross-sectional study conducted between March 2020 and March 2021 in four regions of Cameroon, Southwest, Littoral, Center and West, a total of 1119 fecal samples of children (n = 1119) were collected and genetically analyzed. This study aimed to assess the genetic diversity of Cryptosporidium strains circulating in this patient cohort in Cameroon. Using modified Ziehl–Neelsen fecal smear staining, an overall prevalence of 8.5% (96/1119) was recorded. PCR analysis revealed a prevalence of 15.4% in the Center, 7.2% in the Littoral, 10.5% in the West, and 13.1% in the Southwest regions. Molecular analysis identified Cryptosporidium. hominis and Cryptosporidium parvum as circulating species, with all subtype families suggesting anthroponotic transmission. No zoonotic subtypes of C. parvum were detected. These findings confirm that cryptosporidiosis transmission in Cameroon is primarily anthroponotic. Nonetheless, much larger epidemiological surveys, including other patient cohorts, are necessary for final confirmation of this statement.

Despite several decades of mass drug administration and elimination-related activities, human onchocerciasis still represents a major parasitic threat in endemic regions. Among the challenges encountered by the elimination program is the lack of a suitable diagnostic tool that is accurate and non-invasive. Currently used methods are either invasive or not suitable for monitoring large numbers of patients. Herein, we describe the identification and characterization of Onchocerca volvulus heat shock protein 70 (OvHSP70) as a novel diagnostic biomarker for human onchocerciasis, which can directly be detected in urine samples of infected patients. This nematode-specific antigen was identified through LC-MS after differential SDS-PAGE using urine-derived protein extracts from O. volvulus-infected patients in Cameroon. Polyclonal antibodies generated in rabbits after cloning and expression of OvHSP70 in Escherichia coli reliably differentiated between urine samples from infected- and uninfected patients in a hypoendemic area of human onchocerciasis. These results provide an excellent basis for further development of a non-invasive and scalable diagnostic assay for human onchocerciasis using urine samples. Such a urine-based diagnostic assay will be of major importance for the elimination program of human onchcerciasis in endemic countries.

HIV‐associated pulmonary arterial hypertension (HIV‐PAH) remains one of the most consequential cardiopulmonary complications in people living with HIV (PLWH), persisting despite expanded antiretroviral therapy (ART) coverage. Although contemporary hemodynamic criteria define pulmonary hypertension (PH) as mean pulmonary arterial pressure (mPAP) > 20 mmHg and pulmonary arterial hypertension (PAH) as pre‐capillary physiology confirmed by right heart catheterization (mPAP > 20 mmHg, pulmonary arterial wedge pressure ≤ 15 mmHg, pulmonary vascular resistance > 2 Wood units), global epidemiologic certainty remains uneven. In high‐income settings, prospective screening paradigms incorporating catheter confirmation estimate HIV‐PAH prevalence at approximately 0.5%, exemplified by the multicenter French study reporting 0.46%. In contrast, in sub‐Saharan Africa—home to more than 26 million PLWH—the population prevalence of catheter‐confirmed HIV‐PAH remains undefined, with echocardiography‐based studies in symptomatic cohorts reporting substantially higher rates of elevated pulmonary pressures. Mechanistically, HIV‐PAH is best conceptualized as a multi‐hit pulmonary vasculopathy driven by viral proteins (Tat, Nef, gp120), chronic immune activation, endothelial dysfunction, oxidative stress, dysregulated endothelin signaling, and growth‐factor pathways, with amplification by endemic co‐factors and host susceptibility. Clinically, HIV‐PAH is a “clinically nonspecific phenotype”, frequently obscured by tuberculosis‐related lung disease, anemia, left heart disease, and other causes of dyspnea in resource‐limited settings. Early recognition is critical because prognosis depends on preservation of right ventricular function. A practical, resource‐appropriate strategy is required: heightened clinical suspicion, echocardiography‐anchored detection, systematic exclusion of alternative PH etiologies, rational biomarker use, and referral pathways to right heart catheterization where feasible. ART optimization is necessary but insufficient; PAH‐targeted therapies can improve functional and hemodynamic outcomes, though HIV‐specific randomized evidence remains limited. Implementation science and mechanism‐informed research in endemic regions are urgently needed to close the diagnostic and therapeutic gap.

Background/Objectives: Pulmonary hypertension associated with chronic lung disease remains difficult to diagnose, phenotype, and manage because vascular remodeling, parenchymal lung injury, hypoxemia, inflammation, fibrosis, and right ventricular dysfunction often coexist. Natriuretic peptides are widely used as cardiopulmonary biomarkers, but the receptor-level role of natriuretic peptide receptor-C, encoded by NPR3, remains incompletely defined. This scoping review mapped original empirical evidence on NPR-C/NPR3 and related C-type natriuretic peptide biology in pulmonary hypertension, chronic lung disease, pulmonary vascular remodeling, and right ventricular adaptation. Methods: This scoping review was conducted and reported in accordance with PRISMA-ScR, with applicable PRISMA 2020 reporting elements addressed where relevant to a scoping review. Searches of PubMed/MEDLINE and APA PsycINFO identified 72 records. After removal of 2 duplicates, 70 records underwent title and abstract screening. Forty-two records were excluded at this stage, and 28 reports were sought for full-text retrieval. All reports were retrieved and assessed for eligibility. Eleven reports were excluded at full-text review, leaving 17 original studies for inclusion in the evidence map. Reviews, meta-analyses, editorials, commentaries, protocols, and non-original reports were excluded from the synthesis. Results: The included studies comprised clinical biomarker studies, transcriptomic and receptor-expression analyses, experimental pulmonary hypertension models, chronic lung injury or fibrosis models, and pulmonary vascular cellular studies. Human evidence directly addressing chronic lung disease-associated pulmonary hypertension was limited and largely biomarker-centered, with CNP or NT-proCNP signals suggesting potential relevance to pulmonary vascular stress but without definitive NPR-C/NPR3 validation. Experimental studies supported biologic plausibility, linking CNP/NPR-C-related pathways to endothelial function, pulmonary vascular remodeling, smooth muscle and fibroblast behavior, hypoxic signaling, fibrosis, and right ventricular remodeling. However, findings varied across models, and receptor-specific attribution to NPR-C/NPR3 was often incomplete. Conclusions: Current evidence suggests that NPR-C/NPR3 is a biologically plausible but not yet clinically validated pathway in pulmonary hypertension associated with chronic lung disease. The strongest gap is the absence of prospective human studies integrating invasive hemodynamics, lung disease phenotyping, CNP/NT-proCNP profiling, NPR3 expression or genetic assessment, receptor-level biology, and right ventricular outcomes. Future studies should determine whether NPR-C/NPR3 can improve phenotyping, risk stratification, or therapeutic targeting in chronic lung disease-associated pulmonary hypertension.