Introduction
All living organisms are vulnerable to substances that cause harm. Most of these organisms can protect themselves against health threats with chemical and physical barriers. Although pathogens are potentially harmful, they cannot invade or attack living things since the ability to attack requires susceptible victims (17). For example, the viruses causing infections such as AID in human beings may not affect animals such as mice or cats. Similarly, humans are not susceptible to infections that hurt some animals, and this variation is explainable by the immune response. Immunology is the study of the immune system in humans, and this is a vital and complex branch of biological science (8). Many variables interact to balance an immune system, including diet, medical interventions, and age. The purpose of this paper is to address the effects of age and aging on the immune response to diseases such as COVID-19.
Immunology and Immune System
Before addressing human immunity, it is vital to acknowledge the discipline that deals with the immune system and the study of variable factors. Individuals who work closely with animals are exposed to risks of contracting zoonotic illnesses, which are infections transmissible to humans (17). As stated earlier, immunology is a branch of science concerned with the function and structure of the human immune system (8). In this field, the focus is on maintaining and restoring a natural balance of human immune response by engaging in public health initiatives such as vaccination to promote a healthy lifestyle. Moreover, diseases caused by immune system dysfunction are studied, and new treatments to manage or cure conditions are developed by altering immune system functionality. Usually, immunologists have a crucial role in developing and testing vaccines, and currently, the main effort is directed to develop a cure for COVID-19.
Human beings possess a primitive response to diseases to which they are susceptible. Such a defense is known as natural or innate immunity. The immune system refers to a network of cells, tissues, and organs working to protect the body against invaders. External threats are primarily from microbes such as germs and infectious organisms, including bacteria, parasites, or fungi (17). Since the human body has an ideal environment for multiple microbes, they attempt to break in while the immune system works by keeping them out. In case of dysfunction by the immune system, a torrent of diseases such as allergy, AIDs, or arthritis can be unleashed. The secret of response success is elaborated by dynamics communication between networks in multiple cells.
Typically, the key to a healthy immune system is remarkable potential for different body cells and foreign constituents. Human immune defense coexists peacefully with cells that have distinctive self-makers molecules. As such, when defenders encounter an organism carrying foreign markers, an attack is launched (21). The trigger of such an immune response is referred to as antigen (19). The latter can be a microbe or a part of microbes such as viruses. The behavior of cells from different people explains why tissue transplant rejections are possible. In rare cases, the immune system can mistake identifying oneself and non-self, leading to the launch of an attack on the body’s cells. The resultant effect is an autoimmune disease, and some illnesses such as arthritis or diabetes are examples of this impact (19). In other situations, the immune response can target harmless foreign substances resulting in allergies.
Structure and Function of an Immune System
The organs of the human immune system are located throughout the body. Lymphoid organs are responsible for white blood cells- key players in the defense system. Typically, the bone marrow is soft tissue and the ultimate source of white blood cells, inducing destined immune cells. Lymphocytes travel in the blood vessels, and as cells and fluids are exchanged, the lymphatic system monitors invading microbes. Immune cells enter lymph nodes through lymphatic vessels, and lymphocytes exit the nodes through outgoing vessels (17). While in the bloodstream, they are transported in the entire body to patrol foreign antigens before drifting back to the lymphatic system. According to (12), immune cells start as immature stem cells in the bone marrow and respond to signals while growing into immune cell types such as T-cells and B-cells (4). The latter are the main types of lymphocytes, and while B-cells secrete substances known as antibodies, T-cells’ primary function is to regulate immune responses.
Immunity can be natural or acquired as it becomes recognized that individuals who recovered from a plague would not get it again. In such cases, activated T and B cells become memory cells such that, when a person encounters a similar antigen, the immune system is automatically set to destroy it. According to (6), human immunity can be strong or weak, long-lasting or short-lived based on the number of antigens and types. Immunity is inheritable or influenced by genes such that when faced with the same antigen, people respond differently. Moreover, an immune response can be sparked by immunization with vaccines that contain microorganisms treated to provoke an immune response. In other scenarios, immunity is transferred from one person to another through serum injections rich in antibodies against certain microbes (17). For instance, an immune serum is administered to protect travelers to regions where hepatitis A is common.
Acquired immunity is also known as an adaptive response, and unlike the innate, which attacks upon identification of general threats, adaptive is activated. The acquired immune is much slower to respond to infections than the natural system that is ready to fight. Since adaptive immune can learn and recall pathogens, there is a long-lasting defense to protect against recurring infections. In case the immune system encounters new threats, some antigens are memorized, and the concept of immune memory is enhanced by the body’s ability to create antibodies for various pathogens (17). An excellent illustration of immunological memory is revealed through vaccinations. Vaccination against viruses can be made using active but weakened viruses, attenuated, or inactive parts. Through vaccinations, the body is exposed to the antigen needed to produce antibodies for the virus. With more antibodies, it becomes easier for human beings to fight new diseases or conditions that make the body not to function normally.
Age and Aging Immunity
The human immune system has undergone a dramatic aging-relayed transition, which leads to a continuous progression to immunosenescence. The latter refers to the gradual degradation of the human immune system with age (14). The age factor alters the capacity to respond to infectious illnesses and maintain long-term immune memory from infection or vaccination. An excellent example is chickenpox which when individuals are infected during childhood, they develop a lifelong immunity until old age, where immune memory fails after shingles develop (1). Ideally, age-associated immune deficiency is the primary factor in increased morbidity and mortality in the elderly population.
The aging immune system has a weak ability to protect against infections, and the body fails to support the healing or recovery process. Even with vaccine interventions, the body of older persons might respond less as it is impaired. The inflammatory responses mediated by the innate defense system gain intensity to render older people the susceptibility to organ damaging immunity. As people age, bodies produce inflammation as a protective mechanism to counter the weak immune system. While the impact of aging on innate immunity is insufficiently known, progress has been made to determine the molecular process behind the aging of T cells. In studies with rheumatoid arthritis (RA) patients, T-cells aging was observed to be considerably faster (11). The observation of such behavior enabled the definition of the molecular path underlying the T-cell dysfunction. Having an arthritis condition is linked to shortening life expectancy because of accelerated cardiovascular problems (18). Majorly, diagnosis of RA is connected with the remodeling of the immune system, and T-cells are recognized as aging-related populations.
In other instances, the hallmark of an aging process is associated with the shortening of chromosomal ends due to telomeric sequence repeat. Short telomeres indicate a special case of damaged DNA. In molecular studies with RA T-cells, it has been identified that damage sensing and repair are altered in the aging process (2). Studies in the immune system have demonstrated that adaptive immunity suffers a deterioration with age for lack of intrinsic or extrinsic factors (10). Generating a vigorous immune response in the body depends on the function and repertoire of T-cells. The latter must proliferate to respond to antigen, acquire effectors such as cytokines and migrate appropriately (17). Moreover, the population of T-cell receptors needs to be diverse to recognize the suitable antigenic determinants of pathogens. In young persons, the pool of T-cells fulfills this role, but evidence point that T-cells in aged people are increasingly compromised in effector function.
Naïve T-cells in older people exhibit impaired proliferative responses, graft rejection, and delayed hypersensitivity. The aging population has fewer T-cells, but they are less functional with reduced diversity than equivalent cells in young people. According to the immunological theory, senior human beings grow mild and a generalized autoimmune phenomenon (11). Aging involves complex series of processes that are believed to be controlled by the immune system. As people, they experience changes in physiological forms, including those linked to the immune system. While data reveal that changes in the immune system for elderly persons might be due to symptoms of aging, proponents of the immunological model assert that the opposite is true. Theorists believe that the common symptom of aging result from changes in immune function.
The immune system comprises cells, organs, and substances which work together to fight against diseases. The thymus, tonsils, bone marrow, or lymphatic systems produce or transport cells such as antibodies and interferon (17). As people age, critical cells in the immune network reduce in number and become less functional. Although the number of lymphocyte cells remains relatively constant with age, their portion proliferates, and functionality declines. In medical interventions such as cancer treatment, T-cells can be destroyed and take longer in older people to regenerate. Beyond making people more prone to bacterial or viral infections, changes in the immune system significantly impact (17). Interleukins that serve as messengers to relay signals of regulating immune responses are inhibited.
Effects of Age and Aging on Covid-19 Immunity
Coronaviruses are family evolved infections from a positive sense of single-stranded RNA. Common strains of viruses described in the 1960s, including the human coronavirus (HCoV), are considered mild respiratory pathogens for immunocompetent hosts. Recently, virulent coronavirus strains have merged, where SARS-CoV was initially identified in China and spread to other countries (7). Ten years later, MERS coronavirus was reported in 2013 in the Middle East nations (3). While details of the cause of disease spread are studied, animals such as bats appear to be potential reservoirs (3). To address the challenges imposed by aspects of the SARS virus is paramount, given the current resurgence of new cases of COVID-19.
Most COVID-19 cases are reported to be mild, as some patients may not exhibit clinical manifestation after SARS-CoV-2 infection. However, the asymptomatic persons can be the source of infection spread, given the number of individuals who have tested positive. Artificial intelligence and machine learning have helped address emerging evidence when screening and diagnosing the infection. For severe COVID-19 illnesses, primary risk factors include age, smoking, comorbid conditions such as diabetes. Agreeably, overwhelming evidence across the globe point that age is the most significant risk factor for infection and related adverse outcomes.
Concerning this situation, immunity is a cornerstone of the host-pathogen relationship in any infectious illness. Immunity involves interrelated aspects such as immune response, protection, and vulnerability. The level of vulnerability influences innates immunity that is independent of antigen response. If the immune response to the infection is dysregulated, immune pathology may occur, contributing to the pathogenesis of the infection. Since the novel coronavirus is new with no prior immune response, the general population is at risk and susceptible with no herd community. However, under specific situations, older people are more at risk due to compromise on immunological memory.
The immune system is a sophisticated collection of cells and molecules that help eliminate abnormal cells. At an old age, immune cells that respond to infections become slower and less effective. The aged population makes few cells that cannot adequately recognize and respond to new illnesses such as COVID-19. Moreover, aging impacts cell progress in the airway to fight off the virus. At the same time, age is a critical factor associated with the general background of immune activity in what is termed inflammation. A widespread low level of inflammation causes a negative effect on health and hinders specific immune responses to vaccines or infections (5). The phenomena explain why the new virus primarily impacts the elderly population than young people.
On the contrary, since different age groups have distinct living circumstances and behaviors, it is not clear whether older people are more at risk of infection with the SARS-CoV-2. Studies have shown that young people are more likely to reveal no symptoms from the virus than older patients (16). Random tests across the global population depict that infection rates are similar to all age groups suggesting that elderly persons are at risk. A strong correlation between age and falling seriously ill with the novel virus has been observed. The spread of the COVID-19 is not related to how healthy individuals feel, although older people with multiple underlying health complications are at risk. Individuals are old tend to suffer from different symptoms than young people, and hence they are more likely to be hospitalized with COVID-19 than young persons.
During infection by pathogens, the first layer of the immune system- innate immune response-starts to attack the site’s pathogen. For respiratory illnesses such as COVID-19 complications, the part affected by immune response includes the lungs, nose, and trachea. White blood cells attack pathogens and swallow them up before destruction. At microphages break apart the invading cells, pieces are presented to T-cells, which are the immune system’s memory. In case antigen presentation by macrophage is impaired in the old, such result a decline in T-cell activation. The COVID-19 experience in the aging population presents an opportunity for a long-term global demographic challenge (9). Based on projections, there will be many older people in the future, with the number of old surpassing young persons. Consequently, global aging will create widespread public health issues and dramatically widen the burden of noncommunicable illnesses.
Increasing the immune response is an essential consideration as this would help manage microbes that cause illnesses. Amid the current situation of COVID-19, many clinical trials are underway globally to treat the infection. Examples of these immunity-based interventions include anti-viral drugs, therapies to alter immune response, and antibodies (13). Most treatments have been tested on severely ill patients who are hospitalized and aged. On the contrary, much information about the interaction of COVID-19 and the immune system is needed to determine how this is impacted by age (15). Understanding more about components of the immune system and how they work at different ages or disease stages could potentially reveal the way to target overreactive immunity while fighting the infection.
Dietary strategies are proven ways to enhance the immune response in human beings. Although it is uncertain if nutritional factors lead to senescence, the diet approach can impact immune reverse in aged persons (20). In most cases, lack of proper immunity can be attributed to malnutrition, especially in older people. With that, nutritional support can elevate clinical outcomes in this patient population. People need to observe their diet for them to remain strong and healthy. Moreover, regular exercises boost immune function and lower inflammation. Physical activities strengthen the body muscles and bones and could be a crucial lifestyle intervention for aging people.
Conclusion
In summary, this paper has identified that age and aging are critical factors to immune systems in fighting infections such as COVID-19. The primary effect of age and aging on immunity is a reduction in immune cells. As the body age, not many immune cells are produced. Immune cells such as B and T-cells are responsible for fighting viruses and become fewer in the body with age. Another effect of aging on immunity is rising inflammation which is achieved when a body becomes reddened, hot, painful, and swollen caused by the immune system. Chronic inflammation tends to occur with age for reasons such as poor diet, stress, weight gain, or lack of quality sleep. Thus, age is a critical factor to human immunity, and while nothing can be done to the genetic makeup, factors that positively affect the immune system can be controlled
References
Ahmadpoor, P., & Rostaing, L. (2020). Why the immune system fails to mount an adaptive immune response to a COVID‐19 infection. Transplant International, 33(7), 824-825. Web.
Akbar, A. N., & Gilroy, D. W. (2020). Aging immunity may exacerbate COVID-19.Science, 369(6501), 256-257. Web.
Bajaj, V., Gadi, N., Spihlman, A., Wu, S., Choi, C., & Moulton, V. (2021). Aging, immunity, and COVID-19: How age influences the host immune response to coronavirus infections?Frontiers in Physiology, 11, 1-23. Web.
Bektas, A., Schurman, S. H., Sen, R., & Ferrucci, L. (2017). Human T cell immunosenescence and inflammation in aging.Journal of Leukocyte Biology, 102(4), 977-988. Web.
Bonafè, M., Prattichizzo, F., Giuliani, A., Storci, G., Sabbatinelli, J., & Olivieri, F. (2020). Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes.Cytokine & Growth Factor Reviews, 53, 33-37. Web.
Broere, F., & van Eden, W. (2019). T cell subsets and T cell-mediated immunity. In Nijkamp and Parnham’s Principles of Immunopharmacology (pp. 23-35). Springer, Cham. Web.
Butler, M. & Behringer, D., (2021). Behavioral immunity and social distancing in the wild: The same as in humans?BioScience, 20(10), pp.1-10. Web.
Chavan, S. S., & Tracey, K. J. (2017). Essential neuroscience in immunology.The Journal of Immunology, 198(9), 3389-3397. Web.
Chen, Y., Klein, S. L., Garibaldi, B. T., Li, H., Wu, C., Osevala, N. M., Li, T., Margolick, J. B., Pawalec, G., & Leng, S. X. (2020). Aging in COVID-19: Vulnerability, immunity and intervention.Ageing Research Reviews, 101205. Web.
Chung, K. T. (2019). Aging of Immune System.Journal of Life Science, 29(7), 817-823. Web.
Guo, S., Zhu, Q., Jiang, T., Wang, R., Shen, Y., Zhu, X., Wang, Y., Bai, F., Ding, Q., Zhou, X., Chen, G., & He, D. Y. (2017). Genome-wide DNA methylation patterns in CD4+ T cells from Chinese Han patients with rheumatoid arthritis.Modern Rheumatology, 27(3), 441-447. Web.
Ibrahim, D. R., & Michael, M. I. (2021). Effect of aging on the immune status and trace elements.Arab Journal of Nuclear Sciences and Applications, 54(1), 113-119. Web.
Liang, Z., Zhao, Y., Ruan, L., Zhu, L., Jin, K., Zhuge, Q., Su, D., & Zhao, Y. (2017). Impact of aging immune system on neurodegeneration and potential immunotherapies.Progress in Neurobiology, 157, 2-28. Web.
Oh, S. J., Lee, J. K., & Shin, O. S. (2019). Aging and the immune system: The impact of immunosenescence on viral infection, immunity and vaccine immunogenicity.Immune Network, 19(6).1-18. Web.
Polamarasetti, P., & Martirosyan, D. (2020). Nutrition planning during the COVID-19 pandemic for aging immunity.Bioactive Compounds in Health and Disease, 3(7), 109-123. Web.
Rodriguez, I. J., Lalinde, N., LLano, M., Martínez, L., Montilla, M. D. P., Ortiz, J. P., Rodr´ıguez-Boho´rquez, O. M., Velandia-Vargas, E, A., Herna´ ndez, E. D., & Parra-Lopez, C. A. (2020). Immunosenescence study of T cells: A systematic review.Frontiers in Immunology, 11, 3460. Web.
The Immune System (2021). Lecture 11: The immune system revised [PowerPoint slides]. Slide 1-105.
Tobin, S. W., Alibhai, F. J., Weisel, R. D., & Li, R. K. (2020). Considering cause and effect of immune cell aging on cardiac repair after myocardial infarction.Cells, 9(8), 1-32. Web.
Ugolini, M., & Sander, L. E. (2019). Dead or alive: How the immune system detects microbial viability.Current Opinion in Immunology, 56, 60-66. Web.
Venter, C., Eyerich, S., Sarin, T., & Klatt, K. C. (2020). Nutrition and the immune system: A complicated tango.Nutrients, 12(3), 818. Web.
Xu, W., & Larbi, A. (2017). Markers of T cell senescence in humans.International Journal of Molecular Sciences, 18(8), 1742. Web.