Sammuel Shahzad

Abdulsalam et al. (2026) conducted a review entitled "One Health innovations in tropical disease surveillance for a resilient future". The study explores current tropical disease surveillance approaches that adopt a "One Health" perspective. They concluded that an effective 'One Health' strategy should be proactive rather than reactive, incorporating climate intelligence and addressing the behavioral and social drivers of disease, while also being supported by multilateral cooperation and policy continuity. The authors emphasized the importance of cross-sectoral integration to improve the early detection and response to disease. Furthermore, they argue that technologies, including artificial intelligence, genomic sequencing, environmental biosensors, and mobile health platforms, are enhancing the speed and scalability of disease detection, response, and the prevention of cross-species transmission. The study also highlighted the critical need for interdisciplinary education, policy support, and real-time data sharing to build system-wide resilience. They recommend involving local communities in ecologically sensitive tropical issues and in formulating context-specific surveillance strategies. Lastly, they argue that embedding 'One Health' principles into surveillance practices transforms reactive systems into resilient ones. Iqrar et al. (2026) conducted a study entitled "Development and validation of a novel multiplex PCR assay for the detection of Anaplasma, Babesia and Theileria in captive wild ungulates". The researchers developed a multiplex PCR (mPCR) assay to detect Babesia, Theileria and Anaplasma pathogens simultaneously at the genus level in wild ungulates. For piroplasmids (Babesia and Theileria), two pairs of primers were designed using the 18S ribosomal RNA gene. These primers were specific and sensitive and could generate target products of 178 bp for Theileria and 479 bp for Babesia. Additionally, a primer pair targeting the 16S rRNA gene was designed to generate an expected 318 bp product for Anaplasma. These three primer pairs were tested using blood samples collected from 60 captive Gazella bennettii (Family Bovidae) and Axis porcinus (Family Cervidae) from various wildlife parks and zoos in Punjab, Pakistan. The mPCR results produced by these primers were consistent with those from monoplex PCR, with an overall hemoparasites prevalence of 66.66% (40/60). Sequencing of the PCR products confirmed these results, providing a valuable complementary tool for the simultaneous, accurate and routine detection of Anaplasma and piroplasms in endangered wild ungulates. 2026) presented a clinical case report entitled "Sporadic Creutzfeldt-Jakob disease following venison exposure in a chronic wasting disease-endemic region: a zoonotic surveillance perspective". This study involved a thorough evaluation of the clinical progression, diagnostic assessment, and public health investigation of a patient with Creutzfeldt-Jakob disease (CJD), which is a fatal condition caused by prions. The results they published showed that the 72year-old hunter developed progressive rapid dementia and startle myoclonus. During hospitalization, the patient developed posterior reversible encephalopathy syndrome (PRES). Magnetic resonance imaging showed cortical ribboning and diffusion restriction in the basal ganglia, while cerebrospinal fluid biomarkers (RT-QuIC, total tau and 14-3-3) and post-mortem neuropathology confirmed sporadic CJD of the MM1 subtype. The public health implications of the disease were discussed at length, particularly regarding hunters with extensive exposure to cervids. 2026) conducted a study in Qinghai Province, China titled "Mpox-HIV coinfection in a low-incidence setting: epidemiological insights from Qinghai, China". The study examined the epidemiological characteristics and transmission dynamics of mpox-HIV coinfection in a male patient who had sex with men, as well as systemic gaps in surveillance, diagnosis, and the response to the infection. The patient presented with a fever of 39.4°C and the recovery of mpox virus (MPXV) nucleic acid was confirmed following the collection of a nasopharyngeal swab specimen. Further characterization and identification of the virus revealed it to be MPXV clade IIb (formerly known as the West African clade), C.1.1 sub lineage, with the full designation B.1.3.1.1. As the authors suggest, the findings of this study indicate that the most likely route of exposure for the patient was high-risk sexual contact within a social or sexual network, since no history of international travel was recorded. This finding suggests that silent transmission may already be occurring in regions with low incidence. 2026) conducted a study on the rates of SARS-CoV-2 reinfection and its relationship with vaccination status. They retrospectively analyzed data from patients who experienced reinfection during the second and third waves of the pandemic. Of the 458 participants in the study, 62 (13.54%) who had a primary infection were confirmed to have had a reinfection. Furthermore, 60 participants (13%) were asymptomatic, while 398 participants (87%) were symptomatic, with fever being the most frequently observed symptom during both primary (70.3%) and reinfection (72.58%) infections. Lastly, an association was observed between infection status and vomiting symptoms, which was statistically significant (p < 0.01).Carrero and Mosquera's (2026) article was a review of the re-emergence of arboviruses in the Andean-Amazonian corridor in Latin America. Datasets on various vector-borne diseases from selected countries were analyze from 2023 to 2026 to comprehend epidemiological trends of reemerging diseases. The results showed persistence of malaria in Amazonian areas as well as a sustained increase in arboviruses infection such as yellow fever, dengue and chikungunya. For instance, 132 confirmed human cases of yellow fever outbreak was recorded in Colombia...

Oncogenic viruses contribute to approximately 20% of human cancers globally, with their impact falling disproportionately on populations in Sub-Saharan Africa. In this region, cervical cancer, hepatocellular carcinoma, endemic Burkitt lymphoma, and Kaposi sarcoma represent major causes of cancer-related morbidity and mortality, driven by persistent infection with human papillomavirus (HPV), hepatitis B and C viruses (HBV/HCV), Epstein–Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV), and human T-lymphotropic virus-1 (HTLV-1). This review synthesizes current insights into the immunological mechanisms that underpin viral carcinogenesis in Africa, emphasizing how defective viral clearance, chronic immune activation, and immune evasion arise from the convergence of region-specific co-infections, host genetic diversity, and environmental exposures. We examine the mechanistic roles of HIV-associated CD4⁺ T cell depletion, malaria-induced perturbation of antiviral T cell immunity, helminth-driven T helper 2 polarization, and tuberculosis-associated inflammatory signaling in promoting viral persistence and malignant transformation. In addition, the influence of the extensive diversity of African human leukocyte antigens (HLA) and cytokine gene polymorphisms on antiviral immune responses and cancer susceptibility was discussed. We also assessed how virus-associated tumors establish profoundly immunosuppressive microenvironments characterized by impaired antigen presentation and the dominance of immune checkpoint pathways. Finally, we examined how gaps in vaccination, screening, and diagnostic capacity intersect with immunological vulnerability across Africa, contributing to the burden of infection-associated cancers. These challenges position Africa as a critical setting for developing targeted, genotype-inclusive public health interventions and reducing global cancer disparities through advances in immunoprevention and immunotherapy.

Oncogenic viruses contribute to approximately 15–20% of human cancers globally, with their impact falling disproportionately on populations in Sub-Saharan Africa. In this region, cervical cancer, hepatocellular carcinoma, endemic Burkitt lymphoma, and Kaposi sarcoma represent major causes of cancer-related morbidity and mortality, driven by persistent infection with human papillomavirus (HPV), hepatitis B and C viruses (HBV/HCV), Epstein–Barr virus (EBV), Kaposi sarcoma–associated herpesvirus (KSHV), and human T-lymphotropic virus-1 (HTLV-1). This review synthesizes current insights into the immunological mechanisms that underpin viral carcinogenesis in Africa, emphasizing how defective viral clearance, chronic immune activation, and immune evasion arise from the convergence of region-specific co-infections, host genetic diversity, and environmental exposures. We examine the mechanistic roles of HIV-associated CD4⁺ T cell depletion, malaria-induced perturbation of antiviral T cell immunity, helminth-driven T helper 2 polarization, and tuberculosis-associated inflammatory signaling in promoting viral persistence and malignant transformation. In addition, the influence of the extensive diversity of African human leukocyte antigens (HLA) and cytokine gene polymorphisms on antiviral immune responses and cancer susceptibility was discussed. We also assessed how virus-associated tumors establish profoundly immunosuppressive microenvironments characterized by impaired antigen presentation and the dominance of immune checkpoint pathways. Finally, we examined how gaps in vaccination, screening, and diagnostic capacity intersect with immunological vulnerability across Africa, contributing to the burden of infection-associated cancers. These challenges position Africa as a critical setting for developing targeted, genotype-inclusive public health interventions and reducing global cancer disparities through advances in immunoprevention and immunotherapy.

Wild animals are essential for preserving ecological balance and supporting economic stability. Nonetheless, they are at risk of extinction. Among the factors contributing to this endangerment are pathogens carried by blood-sucking arthropods, especially ticks. Hemoparasites such as Anaplasma, Babesia, and Theileria are spread to wildlife, livestock, and humans mainly by ticks. These intraerythrocytic parasites are traditionally identified by microscopic examination of blood smears stained with Giemsa. However, this method does not always accurately identify coinfections of hemoparasites. Moreover, detecting low levels of parasitism remains a challenge, making it unsuitable for timely diagnosis and predisposing wild animals to possible outbreaks, especially in captive settings. In this study, a multiplex polymerase chain reaction (mPCR) assay was developed to simultaneously detect Anaplasma, Babesia, and Theileria at the genus level in wild ungulates. Three pairs of specific, sensitive primers were designed based on the 16S ribosomal RNA gene (Anaplasma species) and the 18S ribosomal RNA gene (Babesia and Theileria) to generate target products of 318 bp for Anaplasma, 479 bp for Babesia , and 178 bp for Theileria. Blood samples were collected from a total of 60 captive Gazella bennettii (family Bovidae) and Axis porcinus (family Cervidae) from various zoos and wildlife parks in Punjab, Pakistan. To increase sample diversity and size, both families were included in the sampling process. A total of 40/60 (66.66%) samples tested positive, which were evaluated by PCR. Total genomic DNA was extracted for molecular detection by PCR. Three sets of newly designed primers based on genus were used to optimize multiplex PCR for melting temperature and crosslinking among primers. The multiplex PCR assay produced results consistent with monoplex PCR when using the newly designed primers. We detected hemoparasitic infections in 65% of samples, with infection rates of 25% for Anaplasma, 0% for Babesia, and 40% for Theileria. Downstream sequencing also confirmed these PCR results. This assay is a valuable complementary tool for routine, simultaneous, early, and accurate detection of Anaplasma, Babesia, and Theileria, supporting efforts to reduce indiscriminate antibiotic use, control antibiotic resistance, and protect endangered wild ungulates.

Antibodies are highly specialized glycoproteins produced by B cells in response to antigenic stimulation. They are a major component of the adaptive immune system and play a key role in host defenses by detecting, neutralizing, and eliminating foreign antigens. Over the years, their roles have transcended mere immune biomarkers due to their unique specificity, affinity maturation, and structural versatility, making them indispensable tools in biomedical research, including vaccine design, therapeutic development, and diagnostics. In this work, we examine the structural and functional basis of antibody bioactivity while highlighting key engineering strategies, including Fc modification, glycosylation engineering, and the development of novel antibody formats. We also considered the application of engineered antibodies in infectious disease and cancer prevention and treatment, focusing on current challenges, and proposing emerging directions that position antibody engineering as a transformative approach in future biomedical research and innovation.

Nutritional immunity is a major facet of host defense, wherein the host immune system strategically limits pathogen access to critical nutrients, including iron, zinc, vitamins, lipids, and amino acids, to repress microbial proliferation and virulence. This review provides a comprehensive synthesis of the molecular mechanisms that power nutrient immunity, including metal homeostasis, nutrient competition, transporter modulation, hormonal regulation, and direct antimicrobial actions. We examine nutrient-specific strategies employed by the host, such as iron-withholding mechanisms, vitamin deprivation, and copper-mediated toxicity. We also explore how diverse pathogens, including extracellular, intracellular, and eukaryotic pathogens, adapt to these hostile nutritional landscapes through siderophore diversification, regulatory integration, and metabolic rewiring. Comparative genomic analyses reveal convergent evolution in nutrient acquisition systems, illuminating the dynamic arms race between host restriction and microbial evasion. We examine the immunological mechanisms that regulate nutritional immunity. Further, we discuss the translational potential of nutritional immunity, cutting across nutrient-based therapies, host-directed interventions, and emerging diagnostic biomarkers. Finally, we suggest future directions that synergize nutritional immunity with microbiome ecology, global malnutrition, and personalized medicine. By elucidating the interconnection between metabolism and immunity, this review highlights the therapeutic promise of starving or toxifying the pathogen to save the host.

Nutritional immunity is a major facet of host defense, wherein the host immune system strategically limits pathogen access to critical nutrients, including iron, zinc, vitamins, lipids, and amino acids, to repress microbial proliferation and virulence. This review provides a comprehensive synthesis of the molecular mechanisms that power nutrient immunity, including metal homeostasis, transporter modulation, hormonal regulation, and direct antimicrobial actions. We examine nutrient-specific strategies employed by the host, from iron withholding mechanisms to vitamin deprivation and copper-mediated toxicity. We also explore how diverse pathogens, including extracellular, intracellular, and eukaryotic, adapt to these hostile nutritional landscapes through siderophore diversification, regulatory integration, and metabolic rewiring. Comparative genomic analyses reveal convergent evolution in nutrient acquisition systems, illuminating the dynamic arms race between host restriction and microbial evasion. Further, we discuss the translational potential of nutritional immunity, cutting across nutrient-based therapies, host-directed interventions, and emerging diagnostic biomarkers. Finally, we suggest future directions that synergize nutritional immunity with microbiome ecology, global malnutrition, and personalized medicine. By elucidating the interconnection between metabolism and immunity, this review highlights the therapeutic promise of starving the pathogen to save the host.

Ticks and tick-borne diseases (TBDs) are escalating health and veterinary threats in the Global South, driven by environmental change, human activity, and socioeconomic vulnerability. Ticks transmit bacterial, viral, and protozoal pathogens, causing significant public health and economic burdens. Climate shifts and land-use changes have expanded tick habitats, intensifying disease transmission. This review examines the distribution of major tick species in the Global South and explores how ecological disruptions influence disease dynamics. Regional case studies from Africa, the Middle East, and South Asia highlight the impact on human health, livestock productivity, and food security. Addressing this growing threat requires integrated One Health strategies, improved public awareness, enhanced veterinary services, and investment in surveillance and vaccine development. International cooperation and strong policy frameworks are vital to mitigate the spread and impact of TBDs.

Wildlife animals have integral significance in ecological and economic stability. They are becoming extinct. One of the key roots of endangerment is tick-borne diseases. Anaplasma, Babesia, and Theileria are major parasites transmitted by obligatory hematophagous arthropods known as ticks to wildlife, livestock, and humans. In the current study, the creation of novel primers and optimization of a multiplex PCR assay to detect hemoparasites were done. Blood samples were collected from a total of 60 captive Gazella bennettii, family Bovidae, and Axis porcinus, family Cervidae, from different wildlife parks and zoos in Punjab, Pakistan. Both families were targeted during sampling to increase the sample count and obtain a variety of ungulates. Microscopy was performed using the Giemsa staining method, and 40 samples tested positive, which were then proceeded with PCR. Total genomic DNA was extracted for molecular detection by PCR. This study comprised three sets of newly designed primers based on genus to optimize multiplex PCR for melting temperature and crosslinking among primers. The results of our multiplex PCR assay were completely consistent with monoplex PCR using newly designed primers. Results of multiplex PCR revealed the presence of total hemoparasitic species infection in 65% of samples, whereas individual infections of Anaplasma, Babesia, and Theileria were recorded as 25%, 0%, and 40%, respectively. PCR provided accurate results supported by sequencing. This multiplex PCR assay provides a valuable complementary tool in routine, simultaneous, early, and accurate detection of Anaplasma, Babesia, and Theileria genera that helps control antibiotic resistance and save endangered species. Wildlife animals have integral significance in ecological and economic stability. They are becoming extinct. One of the key roots of endangerment is tick-borne diseases. Anaplasma, Babesia, and Theileria are major parasites transmitted by obligatory hematophagous arthropods known as ticks to wildlife, livestock, and humans. In the current study, the creation of novel primers and optimization of a multiplex PCR assay to detect hemoparasites were done. Blood samples were collected from a total of 60 captive Gazella bennettii, family Bovidae, and Axis porcinus, family Cervidae, from different wildlife parks and zoos in Punjab, Pakistan. Both families were targeted during sampling to increase the sample count and obtain a variety of ungulates. Microscopy was performed using the Giemsa staining method, and 40 samples tested positive, which were then proceeded with PCR. Total genomic DNA was extracted for molecular detection by PCR. This study comprised three sets of newly designed primers based on genus to optimize multiplex PCR for melting temperature and crosslinking among primers. The results of our multiplex PCR assay were completely consistent with monoplex PCR using newly designed primers. Results of multiplex PCR revealed the presence of total hemoparasitic species infection in 65% of samples, whereas individual infections of Anaplasma, Babesia, and Theileria were recorded as 25%, 0%, and 40%, respectively. PCR provided accurate results supported by sequencing. This multiplex PCR assay provides a valuable complementary tool in routine, simultaneous, early, and accurate detection of Anaplasma, Babesia, and Theileria genera that helps control antibiotic resistance and save endangered species.

Antiphospholipid syndrome (APS), also known as Hughes syndrome, is a systemic autoimmune disorder characterized by recurrent thrombosis and pregnancy complications, accompanied by the presence of antiphospholipid antibodies (aPLs). These antibodies target anionic phospholipids or protein–phospholipid complexes within cell membranes, contributing to the underlying mechanisms of the disease. Although anticoagulation therapy remains the cornerstone of APS management, it often fails to prevent complications, particularly in obstetric and thrombotic cases. As autoimmune diseases become increasingly linked to alterations in the gut microbiome, this study investigates the complex interaction between gut bacteria and immune modulation in APS. We explore how disruptions in the gut microbiome may influence the development of autoimmune conditions, with a specific focus on APS. By identifying key microorganisms potentially involved in this gut–immune axis, we aim to provide insights into novel preventive and control approaches. Future research should focus on harnessing the gut microbiome to develop more effective treatments that target both the immune system and microbial populations in APS patients.