Review

Potential infectious agents and the human diseases

Ibraheem Ashankyty 1,*

1    Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah 22254, Saudi Arabia.

*    Correspondence: ishankyty@kau.edu.sa (I.A.)

Citation:  Ashankyty, I.  Potential infectious agents and the human diseases. Glob. Jour. Bas. Sci. 2025, 1(6). 1-11.

Received: March 13, 2024

Revised: April 05, 2025

Accepted: April 07, 2025

Published: April 08, 2025

doi: 10.63454/jbs20000026

ISSN: 3049-3315

Volume 1; Issue 6

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Abstract: Infectious diseases remain a leading cause of morbidity and mortality worldwide, driven by a wide range of potential infectious agents, including bacteria, viruses, fungi, protozoa, and helminths. These pathogens can invade and multiply within human hosts, causing illnesses that range from mild to life-threatening. Emerging and re-emerging infectious diseases, such as COVID-19, Ebola, and antibiotic-resistant bacterial infections, highlight the dynamic interaction between humans, microbes, and environmental factors. Despite advances in surveillance and diagnostics, critical gaps persist in understanding the molecular mechanisms of zoonotic spillover, host adaptation, and the drivers of pathogenicity in high-risk viruses (e.g., Nipah, Hendra). Zoonotic transmission, global travel, urbanization, and climate change contribute to the increased incidence and spread of infectious agents. Understanding the biology, transmission pathways, and pathogenic mechanisms of these agents is crucial for developing effective prevention, diagnosis, and treatment strategies. This review provides an overview of major classes of infectious agents, the diseases they cause, and the global challenges in managing infectious threats to public health, and environmental factors.

Keywords: Zoonotic spillover; Emerging infectious diseases; BSL-4 pathogens; One Health; Pandemic preparedness; Viral pathogenesis

 

1. Introduction

Infectious diseases have shaped human history, posing persistent threats to health and survival across populations. These diseases are caused by pathogenic microorganisms—commonly referred to as infectious agents—including viruses, bacteria, fungi, protozoa, and parasitic worms (helminths). When these agents breach the body’s natural defenses, they can multiply and disrupt normal physiological functions, leading to a wide spectrum of clinical manifestations[1-7]. The severity of these diseases varies from mild, self-limiting infections to severe, chronic, or even fatal conditions. Zoonoses, or zoonotic diseases, are infectious illnesses that can naturally spread from animals to people. These illnesses may be brought on by parasites, fungus, viruses, or bacteria (Figure 1). Direct contact with infected animals, consuming tainted food or water, breathing in airborne particles, or being carried by vectors like mosquitoes or ticks are just a few of the ways that zoonotic pathogens can spread. Throughout history, zoonotic infections have caused multiple outbreaks and pandemics, posing serious risks to both public health and international stability. Rabies, avian influenza (H5N1), Ebola virus disease, and the ongoing COVID-19 pandemic brought on by the SARS-CoV-2 virus are a few examples of well-known zoonotic illnesses[8-12].

Figure 1. Infectious diseases and the respective causative agents.

The global burden of infectious diseases remains significant, particularly in low- and middle-income countries where access to healthcare and sanitation may be limited. Meanwhile, globalization, increased international travel, urban overcrowding, and climate change have facilitated the emergence and re-emergence of infectious diseases in new regions. Additionally, the rise of antimicrobial resistance and zoonotic spillovers—where diseases jump from animals to humans—pose critical challenges to public health systems worldwide[13-17].

This paper aims to explore the various classes of infectious agents, examine notable human diseases associated with each, and discuss the mechanisms of transmission, pathogenesis, and control. By understanding the biology and behavior of these pathogens, we can better prepare for current and future outbreaks and improve strategies for prevention, surveillance, and treatment.

To summarize the current form of knowledge on zoonotic and high-risk pathogens, this review employs a systematic approach. The concentration is on BSL-4 agents (e.g., Nipah, Hendra, Ebola) as emerging threats. We conducted a search of PubMed, Web of Science, and WHO (https://www.who.int/publications/i/item/9789240108462) outbreak reports between January 2000 and April 2025, utilizing keywords such as “zoonotic spillover,” “BSL-4 pathogens,” “Nipah virus transmission,” and “One Health interventions.” Peer-reviewed articles, outbreak reports, and consensus guidelines were included in the study, except for non-pathogenic microorganisms and non-English publications. The analysis emphasizes mechanistic insights into cross-species transmission and deficits in outbreak preparedness.

  1. Transmission Routes of Zoonotic Pathogens

Zoonotic diseases, or zoonoses, are infectious diseases that are transmitted between animals and humans. These diseases can be caused by a wide variety of pathogens, including viruses, bacteria, parasites, and fungi. They are transmitted through four primary mechanisms. The initial method is direct contact, which entails physical interactions with infected animals, such as bites, scratches, or exposure to mucous membranes[18]. Rabies, which is contracted through animal wounds [52], and the Nipah virus, which is transmitted through bat secretions[19], are notable examples of this transmission method. The second mechanism is indirect contact, in which individuals are exposed to contaminated environments, such as soil, water, and fomites, or animal products such as meat and milk. This route of transmission is exemplified by anthrax[20], which can develop from particles in the soil, and avian influenza, which is frequently observed in poultry markets[21]. The third is vector-borne transmission, which is facilitated by arthropods including mosquitoes, ticks, and fleas. For example, the West Nile virus is predominantly transmitted by mosquitoes [22], whereas Lyme disease is transmitted through tick bites[22]. Finally, airborne transmission is the result of the inhalation of aerosols or respiratory secretions from infected animals or humans[23, 24]. This method is exemplified by SARS-CoV-2, which is a bat-derived virus that is transmitted between humans[25], and Hantavirus, which can be contracted through aerosols from rodent excreta[26].

 

Table 1. Key zoonotic transmission routes and pathogen examples

Route Pathogen Reservoir Host Key References
Direct contact Rabies virus Dogs, bats [18, 27, 28] 
Nipah virus Fruit bats [19]
Indirect contact Bacillus anthracis Soil, livestock [20]
H5N1 influenza Poultry [21]
Vector-borne West Nile virus Birds [29]
Borrelia burgdorferi (Lyme) Deer, rodents [22]
Airborne SARS-CoV-2 Bats, pangolins [25]
Andes hantavirus Rodents [26]

Many of the most significant infectious disease outbreaks in recent history have been zoonotic in origin. Examples include COVID-19(caused by SARS-CoV-2, likely originating from an animal reservoir), Ebola virus disease, avian influenza (bird flu), rabies, and bovine tuberculosis. Zoonotic pathogens often originate in wildlife, where they may circulate harmlessly until mutations or environmental changes allow them to infect humans, sometimes leading to widespread outbreaks or pandemics[9, 30-33].

Factors contributing to the emergence and spread of zoonotic diseases include:

  • Deforestation and habitat destruction, bringing humans into closer contact with wildlife.
  • Global travel and trade, which can rapidly spread pathogens across borders.
  • Climate change, which affects the distribution of vector populations.
  • Intensive farming and livestock production, increasing opportunities for cross-species transmission.
  • Wet markets and wildlife trade, which facilitate close contact between humans and diverse animal species.

Preventing and controlling zoonotic diseases requires a multidisciplinary approach known as One Health, which recognizes the interconnection between human, animal, and environmental health. Surveillance, vaccination of animal populations, improved hygiene practices, and public education are all vital tools in reducing the risk of zoonotic disease transmission.

Highly Dangerous BSL-4 Viruses: Unleashing their Lethal Potential.

Zoonotic disease mortality and morbidity have increased for numerous reasons. Possible causes:

Disease transmission from animal to human:

The transmission of zoonotic diseases from animals to humans can occur through different mechanisms. Some diseases can directly infect both animals and humans, while others require an intermediate host or vector to complete their life cycle. Factors such as increased human-animal interaction, changes in ecosystems, urbanization, and global travel contribute to the emergence and spread of zoonotic diseases[7, 29].

  1. Direct contact transmission occurs when an infected animal comes into direct physical contact with a susceptible human.
  2. Indirect contact transmission occurs when a person comes into contact with a contaminated environment or object that carries the infectious agent. This can include contaminated surfaces, soil, water, or food.
  3. Vector-borne transmission involves the use of a living organism, typically an arthropod such as mosquitoes, ticks, or fleas, to transmit the infectious agent from an infected animal to a human host. The vector acts as an intermediary, acquiring the pathogen from an infected animal and subsequently transmitting it to a human during a blood meal.
  4. Airborne transmission occurs when infectious agents are suspended in the air in the form of droplets or dust particles and are inhaled by humans. This mode of transmission is more common for respiratory pathogens, such as influenza viruses, coronaviruses, and tuberculosis bacteria. Disease transmission could happen from human to human.

Some zoonotic diseases can be transmitted from human to human. While the primary transmission route for many zoonotic diseases is from animals to humans, certain infectious agents have the potential to spread between humans through various modes of transmission. When zoonotic diseases establish human-to-human transmission, it can lead to sustained outbreaks and even pandemics.

The consequences of human-to-human transmission of zoonotic diseases can be significant and include:

  1. Pathogenecity: BSL-4
  2. Increased Disease Spread:
    Human-to-human transmission can result in rapid and efficient spread of the disease within communities and across regions. This can lead to larger outbreaks and potentially result in a global pandemic, as seen with diseases like COVID-19 caused by the SARS-CoV-2 virus.
  3. Enhanced Adaptation and Evolution:
    When zoonotic pathogens start spreading directly between humans, they may undergo genetic changes and adaptations that enable better survival and transmission within the human population. This can lead to the emergence of new strains or variants of the disease, potentially affecting disease severity, transmissibility, and response to treatments or vaccines.
  4. Healthcare Burden:
    Human-to-human transmission of zoonotic diseases can place a significant burden on healthcare systems. Increased cases and severe illness can overwhelm healthcare facilities, leading to challenges in providing adequate care, shortages of medical supplies, and increased mortality rates.
  5. Economic Impact:
    Outbreaks resulting from human-to-human transmission of zoonotic diseases can have substantial economic consequences. The costs associated with healthcare, containment measures, travel restrictions, and economic disruptions can be substantial, affecting industries, trade, and global economies.
  6. Social Disruption:
    Disease outbreaks and the measures taken to control them can lead to social disruption and impact daily life. Quarantine measures, travel restrictions, and social distancing can affect communities, businesses, education, and mental well-being.

 

Preventing or minimizing human-to-human transmission of zoonotic diseases requires prompt identification, effective public health measures, and adherence to preventive practices. This includes early detection, contact tracing, isolation or quarantine of infected individuals, promotion of hygiene practices, vaccination, and public awareness campaigns to educate people on disease prevention and control measures.

  1. Drivers of Zoonotic Emergence

Environmental and anthropogenic factors are responsible for the significant increase in the prevalence of zoonotic diseases. This is illustrated by the Nipah virus epidemics in Malaysia, which are associated with the loss of bat habitats. Land-use changes, particularly deforestation, result in wildlife being forced into closer proximity to human settlements[18, 27]. The COVID-19 pandemic in densely populated cities has demonstrated that urbanization further accelerates the transmission of disease. Climate change also plays a critical role in the spread of diseases such as dengue and Zika[34], as it alters vector habitats and facilitates the expansion of mosquitoes. Furthermore, it induces bat migration, which results in the introduction of viruses like the Hendra virus to new regions[35]. This issue is also exacerbated by agricultural intensification; livestock husbandry can act as bridge hosts for pathogens, while moist markets, which combine a variety of species, facilitate viral recombination, as demonstrated by the origins of SARS-CoV-2[25, 36]. These risks are further exacerbated by globalization, as air travel enables the rapid dissemination of pathogens across the globe, as illustrated by the H1N1 influenza outbreak of 2009, and the transportation of pathogens across borders by wildlife trade, as demonstrated by monkeypox incidents[36]. Finally, the challenge posed by endemic diseases is further complicated by the proliferation of drug-resistant bacteria, such as MRSA, as a result of the excessive use of antimicrobials in livestock husbandry[37].

 

Table 2. Key drivers and associated pathogens.

Driver Pathogen Example Impact Key References
Land-Use Change

 

 Deforestation Nipah virus Bat-to-pig-to-human transmission [18, 38]
Urbanization COVID-19 High-density living accelerates spread [39]
 

Climate change

 Hendra virus Expanded bat geographic range [35]
Agricultural Intensification Livestock farming H5N1 avian influenza Poultry-to-human spillover [36]
Wet markets SARS-CoV-2 Cross-species viral recombination [25]
Global travel Zika virus Rapid intercontinental spread [34]
Antimicrobial overuse Drug-resistant Salmonella Treatment failures [37]

Immediately after the discovery of COVID-19, the whole world responded collaboratively to global scale pandemic. There was collaborative scientific   response to the COVID-19 outbreak provided a compelling example of the significance of understanding and preparing for outbreaks[1, 6, 7, 16, 17, 29, 40-48]. The COVID-19 pandemic demonstrated the critical importance of understanding and preparing for outbreaks on a. The world’s response to COVID-19 highlighted several key aspects:

  1. Early Detection and Response:
    The ability to detect and respond promptly to emerging outbreaks is crucial. In the case of COVID-19, rapid identification of the novel coronavirus and its potential to cause severe illness enabled early response efforts. Countries that implemented robust surveillance systems and diagnostic capabilities were better positioned to identify cases, trace contacts, and implement containment measures.
  2. Global Collaboration and Information Sharing:
    The response to COVID-19 emphasized the importance of international collaboration and information sharing. Scientists, researchers, and public health authorities across the globe worked together to share data, research findings, and best practices. International organizations such as the World Health Organization (WHO) facilitated coordination, provided guidance, and disseminated critical information to assist countries in their response efforts.
  3. Public Health Measures:
    COVID-19 prompted the implementation of various public health measures to control the spread of the virus. These measures included widespread testing, contact tracing, quarantine and isolation protocols, travel restrictions, and the promotion of hygiene practices such as handwashing and mask-wearing. These interventions were aimed at reducing transmission, protecting vulnerable populations, and minimizing the burden on healthcare systems.
  4. Vaccine Development and Deployment:
    The development, testing, and deployment of vaccines played a crucial role in mitigating the impact of COVID-19. The global scientific community collaborated to expedite vaccine research and development processes. Regulatory agencies worked to assess vaccine safety and efficacy, and vaccination campaigns were launched worldwide to protect populations and achieve herd immunity.
  5. Socioeconomic Impacts and Recovery:
    The COVID-19 pandemic had profound socioeconomic effects, highlighting the interconnectedness of health and the economy. Lockdowns, travel restrictions, and business closures aimed at controlling the virus resulted in economic disruptions, job losses, and financial strain. Governments and organizations implemented various support measures, stimulus packages, and recovery plans to mitigate the socioeconomic impacts and facilitate recovery.

 

The response to COVID-19 underscored the need for robust healthcare systems, investment in research and development, and the importance of public health infrastructure. It also highlighted the significance of effective communication, risk communication, and public trust in authorities during times of crisis.

Understanding and preparing for outbreaks are essential to mitigate the impact of future infectious disease threats. This includes investment in surveillance systems, research, healthcare infrastructure, and the development of strategies and protocols for early detection, rapid response, and effective communication. By learning from the COVID-19 experience, the global community can enhance preparedness, strengthen resilience, and better protect public health in the face of future outbreaks[9, 49-53].

As a result, healthcare systems must develop and regularly update comprehensive preparedness plans to address zoonotic disease outbreaks. These plans should include clear protocols for surveillance, early detection, reporting, and response coordination among healthcare facilities, public health agencies, veterinary services, and other stakeholders. Robust surveillance systems, diagnostic capacity, training, infection prevention, public awareness, collaboration, research, and infrastructure are essential for effective response. Healthcare workers should receive training on zoonotic diseases, including their recognition, diagnosis, treatment, and infection prevention measures. Effective risk communication and public awareness are crucial for accurate and timely information. Healthcare systems should support research and development efforts to advance understanding of zoonotic diseases, invest in adequate infrastructure, and participate in global networks like the World Health Organization to facilitate rapid response, resource mobilization, and knowledge exchange during outbreaks.

Zoonotic pathogens undergo significant adaptation to infect humans or cause severe illnesses (Figure 1). Some pathogens may have pre-existing capabilities to infect multiple host species, including humans, without significant adaptations[4, 5, 8, 10, 43, 51, 54-64].

Multiple zoonotic viruses possess the ability to infect a wide range of host species, hence facilitating an intricate transmission cycle and giving rise to outbreaks in both animal populations and human beings. Here are a few illustrations:

  1. Influenza viruses have the ability to infect various animal species, including avian, porcine, equine, and human hosts. Birds, particularly waterfowl, serve as the inherent reservoir for influenza viruses. The presence of a species barrier facilitates the ability of some strains of influenza A viruses to successfully infect humans, hence initiating the occurrence of seasonal flu outbreaks or global pandemics. The H1N1 influenza strain responsible for the 2009 swine flu pandemic originated in swine populations and then transmitted to humans.
  2. The rabies virus is known to infect various mammalian species, including bats, raccoons, skunks, foxes, as well as domesticated animals such as dogs and cats. The virus has an impact on the central nervous system and is transmitted by animal bites. In various regions, dogs predominantly serve as the primary reservoir for rabies transmission to people, although it is worth noting that other wildlife species also possess the potential to transmit this viral disease.
  3. West Nile virus is primarily maintained in a bird-mosquito transmission cycle. The virus can infect various avian species, including reservoir hosts such as migratory birds. Mosquitoes transmit West Nile fever and other debilitating neurological illnesses to humans and other mammals through their feeding on infected birds.
  4. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the specific viral strain responsible for the latest global pandemic of coronavirus disease 2019 (COVID-19). The COVID-19 pandemic is believed to have originated from bats and subsequently transmitted to humans through an intermediary host. The virus has the ability to infect a variety of animal species, including cats, dogs, minks, non-human primates, and humans.

The extensive range of zoonotic infections capable of infecting many host species underscores the imperative to comprehend the intricate dynamics of transmission and surveillance of these diseases in order to effectively manage and mitigate their dissemination.

  1. Case Studies: High-Impact Zoonoses

The intricate relationship between global health consequences, spillover events, and animal reservoirs is illustrated by three catastrophic zoonotic outbreaks. The ACE2 receptor binding mechanism of the SARS-CoV-2 pandemic, which is suspected to have originated from bats with potential intermediate hosts in Wuhan’s wildlife markets, rapidly achieved human-to-human transmission. This resulted in over 7 million deaths worldwide and exposed critical gaps in wildlife trade regulation (https://www.who.int/publications/i/item/9789240108462) [25, 65]. Similarly, the Nipah virus outbreaks in Malaysia (1998-1999) demonstrated the ability of fruit bat (Pteropus spp.) viruses to amplify through domestic pig populations before transferring to humans. These outbreaks resulted in a high mortality rate of 40-75%, which was attributed to neurotropism and occasional human-to-human transmission[19]. Mass culling of pigs during these epidemics resulted in economic losses eclipsing $500 million and continue to recur in South Asia. The 2014-2016 West Africa outbreak of the Ebola virus, in particular, demonstrated the potential for human chains of transmission to result from the bushmeat handling of infected bats. This process resulted in a fatality rate of approximately 50%, which ultimately overwhelmed healthcare systems and expedited the development of vaccines[66, 67]. These case studies collectively emphasize the convergence of ecological disruption, animal husbandry practices, and global connectivity to facilitate the emergence of zoonotic diseases.

 

Table 3. Comparative analysis of high-impact zoonoses

Pathogen Reservoir Host Spillover Event Case Fatality Rate Key Reference
SARS-CoV-2 Bats (likely) Wuhan wet markets, 2019 ~1–3% [25]
Nipah virus Fruit bats Malaysian pig farms, 1998 ~40–75% [19]
Ebola virus African bats Bushmeat contact, West Africa 2014 ~50% (avg.) [67]

If one would pick a virus that can be considered as the next global outbreak threat it will be the Nipah (NiV) and/or Hendra (HeV) viruses. The highly pathogenic NiV and/or HeV viruses are categorized as biological safety level 4 (BSL-4) pathogens. BSL-4 pathogens are characterized by their high risk of causing severe or fatal disease in humans and the absence of effective treatments or vaccines. These pathogens are often exotic or emerging viruses that pose a significant threat to public health and require the highest level of containment. Some examples of BSL-4 pathogens include Ebola virus, Marburg virus, Lassa fever virus, Nipah virus, Crimean-Congo hemorrhagic fever virus, and certain strains of avian influenza viruses (e.g., H5N1 and H7N9). These pathogens have the potential to cause severe disease outbreaks and have substantial public health implications[7, 68-70].

BSL-4 is the highest level of biological safety and is reserved for working with the most dangerous and exotic pathogens for which there is no known cure or treatment. Dealing with BSL-4 pathogens requires the following:

  • Containment Facilities: Dealing with type of viruses required the availability of BSL-4 laboratories. Those type of laboratories have stringent design and operational requirements to ensure maximum containment. These facilities are isolated and have multiple layers of physical containment barriers, including negative air pressure systems, high-efficiency particulate air (HEPA) filters, and airlock systems. The labs have dedicated supply and exhaust systems, and all personnel working inside the facility must adhere to strict one-way entry and exit protocols.
  • Dealing with patients’ samples requires Personal Protective Equipment (PPE): Personnel working with BSL-4 pathogens must wear specialized, full-body, positive-pressure, air-supplied suits or “space suits” designed to provide a complete barrier between the individual and the potentially infectious agents. The suits are equipped with integrated air supply systems, gloves, and self-contained breathing apparatus (SCBA) to ensure protection.

Due to the complexity and high-risk nature of working with BSL-4 pathogens, research and diagnostic activities involving these agents are subject to strict regulatory oversight. International collaborations, sharing of knowledge, and adherence to established guidelines and regulations are essential to maintain safety and prevent accidental releases.

Hantaviruses: Henipaviruses in the family Paramyxoviridae are closely related (WHO, https://www.who.int/publications/i/item/9789240108462). HeV, like NiV, is spread by Pteropus bats, which kill horses and humans. The virus can infect horses through HeV-infected bat urine. Due to their natural reservoirs, fruit bats (Pteropus genus), being widely distributed throughout Asia, henipaviruses represent a substantial threat to human and animal health. They are spread by bats or domestic animals, have a high fatality rate in humans, and have no vaccines or antivirals. Up to now, there is no vaccination or antivirals for humans have been approved for HeV, although one for horses has been released[27, 28, 71].

The Nipah (NiV): The Nipah Virus (NiV) was discovered in Malaysia and Singapore in 1998-1999 after an outbreak of respiratory and neurological disorders in pigs and encephalitis in pig producers. It caused severe disease in both animals and humans[28, 72-74]. Primarily transmitted by fruit bats. The disease can, also, be contracted through direct contact with infected bats or their secretions. The symptoms range from moderate to severe, and the mortality rate is very high. In Malaysia, Singapore, Bangladesh, and India, outbreaks predominantly occur in rural areas where humans encounter infected bats or animals. Supportive care is the primary component of management for affected individuals. The NiV poses a threat to public health, necessitating ongoing surveillance, investigation, and public health interventions. In 1998-19992, Malaysian and Singaporean pig farmers contracted encephalitis and respiratory and neurological from the NiV. The disease cost the economy 1.1 million swine were killed to contain it. NiV-B was found to cause encephalitis in Bangladesh in 2001. Since then, Bangladesh, India, and the Philippines have recorded almost annual NiV infections. Unfortunately, NiV can overcome species barriers and infect humans and animals with little person-to-person transmission19, making them important. Bat, pig, and human contact is the main source of NiV transmission. In Malaysia, pig farms are near fruit trees, where fruit bats live. Domestic pigs catch NiV infection by eating bat-eaten and saliva-laden fruits or drinking bat urine. However, some NiV outbreaks have revealed human-to-human transmissions, primarily from Nipah patients’ secretions. More than 12 hours of exposure to infected individuals’ bodily fluids can cause human-to-human transmission[75-79].

  1. One Health Mitigation Strategies

The One Health framework (Figure 2), which integrates human, animal, and wildlife health, has been instrumental in the prevention of zoonotic hazards. Successful interventions include livestock vaccination programs, such as the introduction of Hendra virus vaccines for horses in Australia and Nipah virus mitigation through pig immunization in Bangladesh, which reduced transmission risk by 75%[18, 80, 81]. As evidenced by China’s post-SARS bat coronavirus monitoring network, which facilitated the early detection of SARS-like viruses, wildlife surveillance systems are equally critical[82, 83]. Policy priorities should prioritize cross-sectoral coordination, which includes the following: (1) the integration of wildlife disease surveillance into national public health programs, (2) the regulation of high-risk interfaces such as wet markets through mandatory animal testing (e.g., Cambodia’s post-COVID-19 wildlife trade reforms), and (3) the establishment of rapid-response protocols for interspecies outbreaks, which should be modeled after the CDC’s One Health Office outbreak task forces[84]. Community engagement, such as Bangladesh’s “Nipah Scouts” program, which instructs producers to identify bat-contaminated fruit, is essential for bridging implementation gaps[85]. The comprehensive approach required to preemptively disrupt zoonotic transmission chains is exemplified by these measures, which are implemented in conjunction with climate-smart agriculture to mitigate human-wildlife conflict.

 

Table 4. Targeted one health interventions for priority zoonotic pathogens

Intervention Pathogen(s) Implementation Example Key Evidence
Livestock Vaccination Nipah, Hendra Bangladesh: Pig immunization programs 75% spillover reduction[80]
Rift Valley fever Sheep/goat vaccination campaigns Outbreak prevention [https://www.who.int/publications/i/item/9789240108462][86]
Wildlife Surveillance Ebola, SARS-like China: Bat coronavirus monitoring network Early virus detection[82]
Avian influenza (H5N1) Global: Migratory bird tracking systems Outbreak forecasting[80]
Market Regulations SARS-CoV-2, MERS Cambodia: Banned high-risk wildlife trade Reduced zoonotic exposure[84]
Community Education Nipah, Rabies Bangladesh: “Nipah Scouts” farmer training 60% behavior change[85]
Vector Control Lyme, West Nile USA: Tick habitat reduction in parks 40% case decline[34, 87]

 

  1. Discussion and Conclusions
    There is an imperative need for coordinated action that is based on One Health principles in response to the increasing threat of zoonotic diseases. Policy priorities must encompass the following: (1) targeted surveillance of Pteropus bat habitats in Southeast Asia to prevent Nipah spillover, (2) standardized protocols for wildlife market biosecurity (e.g., mandatory testing similar to Cambodia’s post-COVID reforms), and (3) global funding mechanisms to expand livestock vaccination in hotspots (e.g., Hendra vaccines in Australia). Nevertheless, the majority of data is derived from outbreak settings, which results in a lack of understanding of asymptomatic infections and early-stage spillover dynamics. This is a critical gap, as evidence suggests that 50% of emerging zoonoses originate from wildlife reservoirs with cryptic circulation[34]. Future research should prioritize mechanistic studies, such as the elucidation of bat immune tolerance to hemipaviruses, which could reveal novel antiviral targets, and AI-driven forecasting models to predict contagion risks using climate, land-use, and viral genomics data. The global community can alleviate the “era of pandemics” by combining targeted interventions, fundamental research, and cross-border collaboration. Infectious agents—including bacteria, viruses, fungi, protozoa, and helminths—continue to pose significant threats to human health worldwide. These pathogens are responsible for a wide array of diseases, ranging from mild infections to severe, life-threatening illnesses. The emergence of new infectious diseases and the resurgence of old ones underscore the dynamic and evolving nature of microbial threats. Factors such as globalization, environmental change, urbanization, and antimicrobial resistance have further complicated efforts to control infectious diseases. Understanding the biology, transmission mechanisms, and pathogenesis of infectious agents is essential for developing effective strategies for prevention, diagnosis, and treatment. Addressing these challenges also requires a collaborative, interdisciplinary approach—such as the One Health framework—that integrates human, animal, and environmental health. Continued research, surveillance, public health preparedness, and education are critical to mitigating the impact of infectious diseases and improving global health outcomes.

Author Contributions: Conceptualization, I.A.; methodology, I.A.; software, I.A.; formal analysis, I.A.; investigation, I.A.; resources, I.A.; data curation, I.A.; writing—original draft preparation, I.A.; writing—review and editing, I.A.; visualization, I.A.; supervision, I.A.; project administration, I.A.; funding acquisition, I.A. The author has read and agreed to the published version of the manuscript.

Funding: Not applicable.

Acknowledgments: We are grateful to the Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia for providing us all the facilities to carry out the entire work.

Conflicts of Interest: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Institutional Review Board Statement: Not applicable.

Informed Consent Statement: Not applicable.

Data Availability Statement: All the related data are supplied in this work or have been referenced properly.

References

  1. Relman, David A., Microbial Genomics and Infectious Diseases. New England Journal of Medicine, 2011. 365(4): p. 347-357.https://doi.org/10.1056/nejmra1003071
  2. Akira, S., S. Uematsu, and O. Takeuchi, Pathogen Recognition and Innate Immunity. Cell, 2006. 124(4): p. 783-801. https://doi.org/10.1016/j.cell.2006.02.015
  3. Alkhalil, A., et al., Gene expression profiling of monkeypox virus-infected cells reveals novel interfaces for host-virus interactions. Virol J, 2010. 7: p. 173. https://doi.org/10.1186/1743-422X-7-173
  4. Bajrai, L.H., et al., Gene Expression Profiling of Early Acute Febrile Stage of Dengue Infection and Its Comparative Analysis With Streptococcus pneumoniae Infection. Front Cell Infect Microbiol, 2021. 11: p. 707905. https://doi.org/10.3389/fcimb.2021.707905
  5. Bardina, S.V., et al., Enhancement of Zika virus pathogenesis by preexisting antiflavivirus immunity. Science, 2017. 356(6334): p. 175-180. https://doi.org/10.1126/science.aal4365
  6. Collaborators, G.B.D.R.F., Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet, 2016. 388(10053): p. 1659-1724. https://doi.org/10.1016/S0140-6736(16)31679-8
  7. Jones, K.E., et al., Global trends in emerging infectious diseases. Nature, 2008. 451(7181): p. 990-3. https://doi.org/10.1038/nature06536
  8. Helmi, N., D. Alammari, and M. Mobashir, Role of Potential COVID-19 Immune System Associated Genes and the Potential Pathways Linkage with Type-2 Diabetes. Comb Chem High Throughput Screen, 2022. 25(14): p. 2452-2462. https://doi.org/10.2174/1386207324666210804124416
  9. Alammari, D., Cytokine Signaling Pathways are involved in Lung Cancer and COVID-19. Global Journal of Basic Science, 2024. 3(1): p. 1-12. https://doi.org/10.63454/jbs20000003
  10. Bajrai, L., et al., A computational approach reveals the critical role of PARK2 gene and the potential infectious pathways and HPV infection in colorectal cancer. Global Journal of Basic Science, 2025. 1(4): p. 1-11. https://doi.org/10.63454/jbs20000013
  11. Islam, S. and M. Tarek, Impact of measles virus infection on immune signaling pathways in human lung cancer cell lines. Global Journal of Basic Science, 2025. 1(5): p. 1-13. https://doi.org/10.63454/jbs20000011
  12. Marothya, D., Potential roles of cytokine signaling. Global Journal of Basic Science, 2024. 1(2): p. 1-4. https://doi.org/10.63454/jbs20000021
  13. Perelson, A.S., L. Rong, and F.G. Hayden, Combination Antiviral Therapy for Influenza: Predictions From Modeling of Human Infections. The Journal of Infectious Diseases, 2012. 205(11): p. 1642-1645. https://doi.org/10.1093/infdis/jis265
  14. Screaton, G., et al., New insights into the immunopathology and control of dengue virus infection. Nature Reviews Immunology, 2015. 15(12): p. 745-759. https://doi.org/10.1038/nri3916
  15. Tildesley, M.J., et al., Insights into mucosal innate responses to Escherichia coli O157 : H7 colonization of cattle by mathematical modelling of excretion dynamics. Journal of The Royal Society Interface, 2012. 9(68): p. 518-527. https://doi.org/10.1098/rsif.2011.0293
  16. Trowsdale, J. and J.C. Knight, Major Histocompatibility Complex Genomics and Human Disease. Annual Review of Genomics and Human Genetics, 2012. 14(1): p. 301-323. https://doi.org/10.1146/annurev-genom-091212-153455
  17. Wang, B., et al., The Human Microbiota in Health and Disease. Engineering, 2017. 3(1): p. 71-82. https://doi.org/10.1016/j.eng.2017.01.008
  18. Plowright, R.K., et al., Prioritizing surveillance of Nipah virus in India. PLoS Negl Trop Dis, 2019. 13(6): p. e0007393. https://doi.org/10.1371/journal.pntd.0007393
  19. Epstein, L.H., et al., Reducing sedentary behavior: the relationship between park area and the physical activity of youth. Psychol Sci, 2006. 17(8): p. 654-9. https://doi.org/10.1111/j.1467-9280.2006.01761.x
  20. Dragon, D.C. and R.P. Rennie, The ecology of anthrax spores: tough but not invincible. Can Vet J, 1995. 36(5): p. 295-301.
  21. Webster, C.D., et al., Short-Term Assessment of Risk and Treatability (START): The case for a new structured professional judgment scheme. Behav Sci Law, 2006. 24(6): p. 747-66. https://doi.org/10.1002/bsl.737
  22. Steere, A.C., et al., Lyme borreliosis. Nat Rev Dis Primers, 2016. 2: p. 16090. https://doi.org/10.1038/nrdp.2016.90
  23. Peiris, J.S., M.D. de Jong, and Y. Guan, Avian influenza virus (H5N1): a threat to human health. Clin Microbiol Rev, 2007. 20(2): p. 243-67. https://doi.org/10.1128/cmr.00037-06
  24. Smith, G.J., et al., Emergence and predominance of an H5N1 influenza variant in China. Proc Natl Acad Sci U S A, 2006. 103(45): p. 16936-41. https://doi.org/10.1073/pnas.0608157103
  25. Zhou, Z., et al., Heightened Innate Immune Responses in the Respiratory Tract of COVID-19 Patients. Cell Host Microbe, 2020. 27(6): p. 883-890 e2. https://doi.org/10.1016/j.chom.2020.04.017
  26. Jónsson, T., P. Pinson, and H. Madsen, On the market impact of wind energy forecasts. Energy Economics, 2010. 32(2): p. 313-320. https://doi.org/10.1016/j.eneco.2009.10.018
  27. Letko, M., et al., Bat-borne virus diversity, spillover and emergence. Nat Rev Microbiol, 2020. 18(8): p. 461-471. https://doi.org/10.1038/s41579-020-0394-z
  28. Aditi and M. Shariff, Nipah virus infection: A review. Epidemiol Infect, 2019. 147: p. e95. https://doi.org/10.1017/S0950268819000086
  29. Pierson, T.C. and M.S. Diamond, The continued threat of emerging flaviviruses. Nature Microbiology, 2020. 5(6): p. 796-812. https://doi.org/10.1038/s41564-020-0714-0
  30. Coyne, C.B. and H.M. Lazear, Zika virus — reigniting the TORCH. Nature Reviews Microbiology, 2016. 14(11): p. 707-715. https://doi.org/10.1038/nrmicro.2016.125
  31. Delorey, T.M., et al., COVID-19 tissue atlases reveal SARS-CoV-2 pathology and cellular targets. Nature, 2021. 595(7865): p. 107-113. https://doi.org/10.1038/s41586-021-03570-8
  32. Long, S., et al., SARS-CoV-2 N protein recruits G3BP to double membrane vesicles to promote translation of viral mRNAs. Nat Commun, 2024. 15(1): p. 10607. https://doi.org/10.1038/s41467-024-54996-3
  33. Mobashir, M., The Understanding of the Potential Linkage between COVID-19, Type-2 Diabetes, and Cancer(s) Could Help in Better Drug Targets and Therapeutics. Comb Chem High Throughput Screen, 2022. 25(14): p. 2370-2371. https://doi.org/10.2174/138620732514220908124350
  34. Bogoch, II, et al., Potential for Zika virus introduction and transmission in resource-limited countries in Africa and the Asia-Pacific region: a modelling study.Lancet Infect Dis, 2016. 16(11): p. 1237-1245. http://dx.doi.org/10.1016/S1473-3099(16)30270-5
  35. Allen, M.R., et al., Net Zero: Science, Origins, and Implications. Annual Review of Environment and Resources, 2022. 47(1): p. 849-887. https://doi.org/10.1146/annurev-environ-112320-105050
  36. Gilbert, J.A., J.K. Jansson, and R. Knight, The Earth Microbiome project: successes and aspirations. BMC Biol, 2014. 12: p. 69. https://doi.org/10.1186/s12915-014-0069-1
  37. Van Boeckel, T.P., et al., Global trends in antimicrobial resistance in animals in low- and middle-income countries. Science, 2019. 365(6459). https://doi.org/10.1126/science.aaw1944
  38. Olivero, J., et al., Recent loss of closed forests is associated with Ebola virus disease outbreaks. Sci Rep, 2017. 7(1): p. 14291. https://doi.org/10.1038/s41598-017-14727-9
  39. Gibb, R., et al., Zoonotic host diversity increases in human-dominated ecosystems. Nature, 2020. 584(7821): p. 398-402. https://doi.org/10.1038/s41586-020-2562-8
  40. Bonaguro, L., et al., A guide to systems-level immunomics. Nat Immunol, 2022. 23(10): p. 1412-1423. https://doi.org/10.1038/s41590-022-01309-9
  41. Casanova, J.-L. and L. Abel, The Genetic Theory of Infectious Diseases: A Brief History and Selected Illustrations. Annual Review of Genomics and Human Genetics, 2012. 14(1): p. 215-243. https://doi.org/10.1146/annurev-genom-091212-153448
  42. Chapman, S.J. and A.V.S. Hill, Human genetic susceptibility to infectious disease. Nature Reviews Genetics, 2012. 13(3): p. 175-188. https://doi.org/10.1038/nrg3114
  43. Chaturvedi, U.C., R. Nagar, and R. Shrivastava, Dengue and dengue haemorrhagic fever: implications of host genetics. FEMS Immunology & Medical Microbiology, 2006. 47(2): p. 155-166. https://doi.org/10.1111/j.1574-695x.2006.00058.x
  44. Feng, Z., et al., A pathogenic picornavirus acquires an envelope by hijacking cellular membranes. Nature, 2013. 496(7445): p. 367-371. https://doi.org/10.1038/nature12029
  45. Jopeace, A.L., et al., Insight and Control of Infectious Disease in Global Scenario. 2012. https://doi.org/10.5772/33481
  46. Morens, D.M., G.K. Folkers, and A.S. Fauci, The challenge of emerging and re-emerging infectious diseases. Nature, 2004. 430(6996): p. 242-9. https://doi.org/10.1038/nature02759
  47. Pikis, A., et al., Optochin Resistance in Streptococcus pneumoniae: Mechanism, Significance, and Clinical Implications. The Journal of Infectious Diseases, 2001. 184(5): p. 582-590. https://doi.org/10.1086/322803
  48. Wang, D., et al., Viral Discovery and Sequence Recovery Using DNA Microarrays. PLoS Biology, 2003. 1(2): p. e2. https://doi.org/10.1371/journal.pbio.0000002
  49. Alammari, D. and N. Helmi, An integrated approach for herbal drugs to target GSK3B and its linkage with melanoma and type-2 diabetes. Global Journal of Basic Science, 2024. 1(2): p. 1-13. https://doi.org/10.63454/jbs20000014
  50. Almowallad, S., R. Jeet, and M. Mobashir, Systems-level understanding of toxicology and cardiovascular system. Global Journal of Basic Science, 2024. 5(1): p. 1-16. https://doi.org/10.63454/jbs20000005
  51. Almowallad, S., R. Jeet, and M. Mobashir, A systems pharmacology approach for targeted study of potential inflammatory pathways and their genes in atherosclerosis. Global Journal of Basic Science, 2024. 6(1): p. 1-12. https://doi.org/10.63454/jbs20000006
  52. Islam, S. and R. Ahmed, Network pharmacological approach to predict the herbal drug targets in Measles Virus infection. Global Journal of Basic Science, 2025. 1(5). https://doi.org/10.63454/jbs200014sa
  53. Jeet, R., Phytomedicine as the alternative drug against the human disease. Global Journal of Basic Science, 2024. 7(1).https://doi.org/10.63454/jbs20000007
  54. Almowallad, S., L.S. Alqahtani, and M. Mobashir, NF-kB in Signaling Patterns and Its Temporal Dynamics Encode/Decode Human Diseases. Life (Basel), 2022. 12(12). https://doi.org/10.3390/life12122012
  55. Bajrai, L.H., et al., Understanding the role of potential pathways and its components including hypoxia and immune system in case of oral cancer. Sci Rep, 2021. 11(1): p. 19576. https://doi.org/10.1038/s41598-021-98031-7
  56. El-Kafrawy, S.A., et al., Genomic profiling and network-level understanding uncover the potential genes and the pathways in hepatocellular carcinoma.Front Genet, 2022. 13: p. 880440. https://doi.org/10.3389/fgene.2022.880440
  57. Huwait, E. and M. Mobashir, Potential and Therapeutic Roles of Diosmin in Human Diseases. Biomedicines, 2022. 10(5).https://doi.org/10.3390/biomedicines10051076
  58. Warsi, M.K., et al., Comparative Study of Gene Expression Profiling Unravels Functions Associated with Pathogenesis of Dengue Infection. Curr Pharm Des, 2020. 26(41): p. 5293-5299. https://doi.org/10.2174/1381612826666201106093148
  59. Borchering, R.K., et al., Impacts of Zika emergence in Latin America on endemic dengue transmission. Nature Communications, 2019. 10(1): p. 5730. https://doi.org/10.1038/s41467-019-13628-x
  60. Cordeiro, M.T., et al., Characterization of a dengue patient cohort in Recife, Brazil. The American journal of tropical medicine and hygiene, 2007. 77(6): p. 1128-34. https://app.readcube.com/library/13da053b-6958-47c0-9554-e2a5ffb811c6/item/66c39f4b-f1d4-4217-83fc-42e7efa90705
  61. Datan, E., et al., Dengue-induced autophagy, virus replication and protection from cell death require ER stress (PERK) pathway activation. Cell Death & Disease, 2016. 7(3): p. e2127-e2127. https://doi.org/10.1038/cddis.2015.409
  62. Guzman, M.G., et al., Dengue infection. Nature Reviews Disease Primers, 2016. 2(1): p. 16055. https://doi.org/10.1038/nrdp.2016.55
  63. Guzman, M.G., et al., Dengue: a continuing global threat. Nature Reviews Microbiology, 2010. 8(Suppl 12): p. S7-S16. https://doi.org/10.1038/nrmicro2460
  64. Kazmi, S.S., et al., A review on Zika virus outbreak, epidemiology, transmission and infection dynamics. Journal of Biological Research-Thessaloniki, 2020. 27(1): p. 5. https://doi.org/10.1186/s40709-020-00115-4
  65. Andersen, K.G., et al., The proximal origin of SARS-CoV-2. Nat Med, 2020. 26(4): p. 450-452. https://doi.org/10.1038/s41591-020-0820-9
  66. Henao-Restrepo, A.M., et al., Efficacy and effectiveness of an rVSV-vectored vaccine in preventing Ebola virus disease: final results from the Guinea ring vaccination, open-label, cluster-randomised trial (Ebola Ca Suffit!). Lancet, 2017. 389(10068): p. 505-518. http://dx.doi.org/10.1016/S0140-6736(16)32621-6
  67. Leroy, E.M., et al., Fruit bats as reservoirs of Ebola virus. Nature, 2005. 438(7068): p. 575-6. https://doi.org/10.1038/438575a
  68. Fillon, M., The social media cancer misinformation conundrum. CA Cancer J Clin, 2022. 72(1): p. 3-4. https://doi.org/10.3322/caac.21710
  69. Van Dijck, C., et al., Emergence of mpox in the post-smallpox era-a narrative review on mpox epidemiology. Clin Microbiol Infect, 2023. 29(12): p. 1487-1492. https://doi.org/10.1016/j.cmi.2023.08.008
  70. Elliott, B., et al., Clostridium difficile infection: Evolution, phylogeny and molecular epidemiology. Infect Genet Evol, 2017. 49: p. 1-11. https://doi.org/10.1016/j.meegid.2016.12.018
  71. Zhao, Y., et al., Cryptococcus neoformans, a global threat to human health. Infect Dis Poverty, 2023. 12(1): p. 20. https://doi.org/10.1186/s40249-023-01073-4
  72. Krishnamoorthy, P.K.P., et al., T-cell Epitope-based Vaccine Design for Nipah Virus by Reverse Vaccinology Approach. Comb Chem High Throughput Screen, 2020. 23(8): p. 788-796. https://doi.org/10.2174/1386207323666200427114343
  73. Devnath, P., et al., The pathogenesis of Nipah virus: A review. Microb Pathog, 2022. 170: p. 105693. https://doi.org/10.1016/j.micpath.2022.105693
  74. Faus-Cotino, J., G. Reina, and J. Pueyo, Nipah Virus: A Multidimensional Update. Viruses, 2024. 16(2). https://doi.org/10.3390/v16020179
  75. Singh, R.K., et al., Nipah virus: epidemiology, pathology, immunobiology and advances in diagnosis, vaccine designing and control strategies – a comprehensive review. Vet Q, 2019. 39(1): p. 26-55. https://doi.org/10.1080/01652176.2019.1580827
  76. Soman Pillai, V., G. Krishna, and M. Valiya Veettil, Nipah Virus: Past Outbreaks and Future Containment. Viruses, 2020. 12(4). https://doi.org/10.3390/v12040465
  77. Talukdar, P., et al., Molecular Pathogenesis of Nipah Virus. Appl Biochem Biotechnol, 2023. 195(4): p. 2451-2462. https://doi.org/10.1007/s12010-022-04300-0
  78. Wang, L., et al., Nipah virus: epidemiology, pathogenesis, treatment, and prevention. Front Med, 2024. 18(6): p. 969-987. https://doi.org/10.1007/s11684-024-1078-2
  79. Wang, Z., et al., Architecture and antigenicity of the Nipah virus attachment glycoprotein. Science, 2022. 375(6587): p. 1373-1378. https://doi.org/10.1126/science.abm5561
  80. Gurley, N., et al., National policy responses to maintain essential health services during the COVID-19 pandemic. Bull World Health Organ, 2022. 100(2): p. 168-170. http://dx.doi.org/10.2471/BLT.21.286852
  81. Peel, T.N., et al., Trial of Vancomycin and Cefazolin as Surgical Prophylaxis in Arthroplasty. N Engl J Med, 2023. 389(16): p. 1488-1498. https://doi.org/10.1056/NEJMoa2301401
  82. Wang, P., et al., Increased resistance of SARS-CoV-2 variant P.1 to antibody neutralization. Cell Host Microbe, 2021. 29(5): p. 747-751 e4. https://doi.org/10.1016/j.chom.2021.04.007
  83. Wang, Z., et al., Naturally enhanced neutralizing breadth against SARS-CoV-2 one year after infection. Nature, 2021. 595(7867): p. 426-431. https://doi.org/10.1038/s41586-021-03696-9
  84. Vora, N.M., et al., Interventions to Reduce Risk for Pathogen Spillover and Early Disease Spread to Prevent Outbreaks, Epidemics, and Pandemics.Emerg Infect Dis, 2023. 29(3): p. 1-9. https://doi.org/10.3201/eid2903.221079
  85. Homaira, N., Will nirsevimab be the holy grail for prevention of respiratory syncytial virus lower respiratory tract infections in infants? Transl Pediatr, 2024. 13(3): p. 525-529. https://doi.org/10.21037/tp-23-53
  86. Wattsb, D.M., et al., Evaluation of a Combined Peste des Petits Ruminants and Rift Valley Fever Live Vaccine in Sheep and Goats. Journal of Vaccines & Vaccination, 2021. 12(3): p. 1-10. https://doi.org/10.35248/2157-7560.21.s14.003
  87. Cavazzana-Calvo, M., et al., Gene Therapy of Human Severe Combined Immunodeficiency (SCID)-X1 Disease. Science, 2000. 288(5466): p. 669-672. https://doi.org/10.1126/science.288.5466.669

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