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An analysis of the SARS-Cov-2 genome shows that it is over 80% similar to the SARS (severe acute respiratory syndrome)-Cov-1 virus that originated in China in 2003 (Keshta et al., 2021). It is a single stranded RNA virus, and the genome encodes four major proteins on the virus’ envelope (outer surface). The protein responsible for human cell infection is the spike (S) protein. The virus enters the lungs through respiratory droplets. Then, this protein binds to the human cell’s receptor for angiotensin-converting enzyme 2 (ACE2), allowing the virus to fuse its envelope with the cell membrane so the virus can enter the cell (Rauf et al., 2020). After entry, the viral genome enters the cytoplasm and is consequently replicated by the human cell’s molecular machinery. An inflammatory response results which can lead to acute respiratory failure or acute respiratory distress syndrome (Alahmari et al. 2023).

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SARS-CoV-2 commonly binds to a protein called ACE2 (angiotensin-converting enzyme 2) (Bohn et al., 2020), which is a protein which affects blood-pressure, hence the increased severity of symptoms in patients with hypertension (Bialek et al., 2020). This protein acts as its ticket for entry into host cells (Walls et al., 2020). Since ACE2 is expressed by type II alveolar cells, those are the host cells infected in the most common pulmonary form of COVID-19. Most notably, this infection causes a deficiency in surfactant (Calkovska et al., 2021), which is a phospholipid-protein complex lining alveoli to decrease surface tension between the air in the alveoli and the water in the cells of the alveoli (Han & Mallampalli, 2015). So whether SARS-CoV-2 causes a dysfunction or a deficiency in the production of surfactant, it can disrupt the respiratory efficiency of a patient. Too little surfactant causes alveolar collapse while too much may prevent gas exchange. Or even an anomalous structure of surfactant like an inconsistent foamy matrix can damage alveolar cells as well as their ability to resist microorganism and particulate damage (Ninham et al., 2022). While energy is expended by the host to compensate for the respiratory complications, infection spreads throughout the body to cause diffuse inflammatory responses, eventual sepsis, and death as a direct result if not from respiratory failure (Siddiqi & Mehra, 2020).

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SARS-CoV-2 is generally agreed to have three stages. Stage I is the early infection stage during which the virus establishes in the host and multiplies mostly in the respiratory system (Siddiqi & Mehra, 2020). This stage is characterized by non-specific symptoms similar to a mild cold such as malaise, fever, and a dry cough. Stage II is split into two types: pulmonary involvement without hypoxia (IIa) and pulmonary involvement with hypoxia (IIb). This is when inflammation begins in the lungs, causing pneumonia, a cough, fever, and possible slight hypoxia. The difference between the subtypes is the severity of hypoxia and whether intervention must be taken for the patient to maintain a healthy SpO2>90% (if high flow oxygen does not help). Interventions include corticosteroids to battle inflammation and mechanical ventilation. Stage III is considered the severe stage as inflammation becomes systemically exaggerated. During this period, the patient’s body is overloaded and cannot match the infection with appropriate T cell levels to fight it. Some T-cells are meant to negatively regulate inflammatory responses specifically, so this is linked to the increase in cytokines and chemokines causing the exaggerated global inflammatory response (Qin et al., 2020).

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While COVID-19 primarily affects the respiratory system, it also affects other organ systems, including the heart, blood vessels, brain, neurons, kidneys, liver, and reproductive organs. For example, it can lead to heart-related problems such as myocarditis, atrial fibrillation, and increased clotting risks, which can persist even after recovery (Merschel 2024). There is also an increased risk of thromboembolic events like strokes. Neurologically, COVID-19 has been linked to issues like fog, cognitive impairment, and in severe cases neuropathy in limbs (Merschel 2024). The gastrointestinal system is also affected, with reports of persistent virus presence and symptoms like nausea and diarrhea, sometimes lasting months post-infection (Merschel 2024). Additionally, kidneys can experience damage, potentially from dehydration during illness or direct viral effects (Merschel 2024).

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It is known that the elderly and immunocompromised are at highest risk of contracting SARS-CoV-2 and having lasting symptoms after recovery (Siddiqi & Mehra, 2020). According to the Nature journal, confirming the presence of long COVID-19 is difficult due to the absence of diagnostics for it and the under-recorded cases of it in EMR systems. It is a status reported predominantly by patient’s themselves who may be mis-identifying symptoms resulting from a separate medical condition (Ghafari et al., 2024). However, the Journal of Infectious Diseases (IDSA), has run an analytical systematic review of 50 studies on long COVID-19 from different populations, regions, sex, and medical status. From the data compiled, it was estimated that global prevalence of long COVID-19 was anywhere from 39-46% (with 95% confidence) about a month out from recovery. However, studies written in languages other than English were excluded from the analysis, and other conditions of exclusion or bias are detailed in the study (Chen et al., 2022).

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Alahmari, A., Krishna, G., Jose, A. M., Qoutah, R., Hejazi, A., Abumossabeh, H., Atef, F., Almutiri, A., Homoud, M., Algarni, S., Alahmari, M., Alghamdi, S., Alotaibi, T., Alwadeai, K., Alhammad, S., & Alahmari, M. (2023). The long-term effects of COVID-19 on pulmonary status and quality of life. PeerJ (San Francisco, CA), 11, e16694–e16694. https://doi.org/10.7717/peerj.16694

Bialek, S., Boundy, E., Bowen, V., Chow, N., Cohn, A., Dowling, N., Ellington, S., Gierke, R., Hall, A., MacNeil, J., Patel, P., Peacock, G., Pilishvili, T., Razzaghi, H., Reed, N., Ritchie, M., & Sauber-Schatz, E. (2020). Severe Outcomes Among Patients with Coronavirus Disease 2019 (COVID-19) — United States, February 12–March 16, 2020. MMWR. Morbidity and Mortality Weekly Report, 69(12). https://doi.org/10.15585/mmwr.mm6912e2

Bohn, M. K., Hall, A., Sepiashvili, L., Jung, B., Steele, S., & Adeli, K. (2020). Pathophysiology of COVID-19: Mechanisms Underlying Disease Severity and Progression. Physiology, 35(5), 288–301. https://doi.org/10.1152/physiol.00019.2020

Bösmüller, H., Matter, M., Fend, F., & Tzankov, A. (2021). The pulmonary pathology of COVID-19. Virchows Archiv : An International Journal of Pathology, 478(1), 137–150. https://doi.org/10.1007/s00428-021-03053-1

Calkovska, A., Kolomaznik, M., & Calkovsky, V. (2021). Alveolar Type II Cells and Pulmonary Surfactant in COVID-19 Era. Physiological Research, 70(2), S195–S208. https://doi.org/10.33549/physiolres.934763

Chen, C., Haupert, S. R., Zimmermann, L., Shi, X., Fritsche, L. G., & Mukherjee, B. (2022). Global Prevalence of Post COVID-19 Condition or Long COVID: A Meta-Analysis and Systematic Review. The Journal of Infectious Diseases, 226(9). https://doi.org/10.1093/infdis/jiac136

FDA. (2022). COVID-19 Test Basics. FDA. https://www.fda.gov/consumers/consumer-updates/covid-19-test-basics

Ghafari, M., Hall, M., Golubchik, T., Ayoubkhani, D., House, T., MacIntyre-Cockett, G., Fryer, H. R., Thomson, L., Nurtay, A., Kemp, S. A., Ferretti, L., Buck, D., Green, A., Trebes, A., Piazza, P., Lonie, L. J., Studley, R., Rourke, E., Smith, D. L., & Bashton, M. (2024). Prevalence of persistent SARS-CoV-2 in a large community surveillance study. Nature, 626, 1–8. https://doi.org/10.1038/s41586-024-07029-4

Han, S. H., & Mallampalli, R. K. (2015). The Role of Surfactant in Lung Disease and Host Defense against Pulmonary Infections. Annals of the American Thoracic Society, 12(5), 765–774. https://doi.org/10.1513/annalsats.201411-507fr

Huang, S., Zhao, S., Luo, H., Wu, Z., Wu, J., Xia, H., & Chen, X. (2021). The role of extracorporeal membrane oxygenation in critically ill patients with COVID-19: a narrative review. BMC Pulmonary Medicine, 21(1), 116. https://doi.org/10.1186/s12890-021-01479-6

Keshta, A. S., Mallah, S. I., Al Zubaidi, K., Ghorab, O. K., Keshta, M. S., Alarabi, D., Abousaleh, M. A., Salman, M. T., Taha, O. E., Zeidan, A. A., Elsaid, M. F., & Tang, P. (2021). COVID-19 versus SARS: A comparative review. Journal of Infection and Public Health, 14(7), 967–977. https://doi.org/10.1016/j.jiph.2021.04.007

Livieratos, A., Gogos, C., & Akinosoglou, K. (2024). Impact of Prior COVID-19 Immunization and/or Prior Infection on Immune Responses and Clinical Outcomes. Viruses, 16(5), 685-. https://doi.org/10.3390/v16050685

Merschel, Michael (2024). Beyond Breathing: How COVID-19 Affects Your Heart, Brain and Other Organs. American Heart Association News. https://www.heart.org/en/news/2024/01/16/how-covid-19-affects-your-heart-brain-and-other-organs

Ninham, B., Reines, B., Battye, M., & Thomas, P. (2022). Pulmonary surfactant and COVID-19: A new synthesis. QRB Discovery, 3(6). https://doi.org/10.1017/qrd.2022.1

Prather, K. A., Wang, C. C., & Schooley, R. T. (2020). Reducing transmission of SARS-CoV-2. Science, 368(6498), 1422-1424. https://doi.org/10.1126/science.abc6197

Qin, C., Zhou, L., Hu, Z., Zhang, S., Yang, S., Tao, Y., Xie, C., Ma, K., Shang, K., Wang, W., & Tian, D.-S. (2020). Dysregulation of immune response in patients with COVID-19 in Wuhan, China. Clinical Infectious Diseases, 71(15), 762–768. https://doi.org/10.1093/cid/ciaa248

Raman, K. (2023). There’s a new updated COVID-19 vaccine just in time for the respiratory virus season. AZ Dept. Of Health Services News. https://directorsblog.health.azdhs.gov/theres-a-new-updated-covid-19-vaccine-just-in-time-for-the-respiratory-virus-season/

Rauf, A., Abu-Izneid, T., Olatunde, A., Khalil, A. A., Alhumaydhi, F. A., Tufail, T., Shariati, M. A., Rebezov, M., Almarhoon, Z. M., Mabkhot, Y. N., Alsayari, A., & Rengasamy, K. R. R. (2020). COVID-19 Pandemic: Epidemiology, Etiology, Conventional and Non-Conventional Therapies. International Journal of Environmental Research and Public Health, 17(21), 8155-. https://doi.org/10.3390/ijerph17218155

Reed, J., & Huthinson, S. (2020). Coronavirus: Warning thousands could be left with lung damage. BBC News. https://www.bbc.com/news/health-53065340

Siddiqi, H. K., & Mehra, M. R. (2020). COVID-19 Illness in Native and Immunosuppressed States: A Clinical-Therapeutic Staging Proposal. The Journal of Heart and Lung Transplantation, 39(5). https://doi.org/10.1016/j.healun.2020.03.012

Walls, A. C., Park, Y.-J., Tortorici, M. A., Wall, A., McGuire, A. T., & Veesler, D. (2020). Structure, function, and antigenicity of the sars-cov-2 spike glycoprotein. Cell, 181(2), 281–292. https://doi.org/10.1016/j.cell.2020.02.058

Wiersinga, W. J., Rhodes, A., Cheng, A. C., Peacock, S. J., & Prescott, H. C. (2020). Pathophysiology, transmission, diagnosis, and treatment of coronavirus disease 2019 (COVID-19): A review. JAMA, 324(8), 782-793. https://doi.org/10.1001/jama.2020.12839

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The lungs are the primary organ impacted by COVID-19. While most individuals with COVID-19 only experience flu-like symptoms caused by inflammation and viral infection, more serious cases can arise. In some severe cases, patients develop long COVID-19, in which symptoms persist for weeks or months after infection (Alahmari et al. 2023). The chief cause is pulmonary damage. The first stage of COVID-19, occurring in the first day, is characterized by edema and damage to the epithelium lining the airways (Bösmüller et al., 2021). Additionally, capillaries become inflamed, and small blood clots (microthrombosis) form in them. During the next one to seven days, COVID-19 can progress (especially in patients with confounding health issues such as obesity or heart disease) to cause diffuse alveolar damage (DAD). This is marked by the formation of hyaline membranes, an abnormal increase in lung cells (pneumocyte hyperplasia), and severe inflammation of lung tissue. These conditions create stress on gas exchange, and acute respiratory distress syndrome occurs (Bösmüller et al.). Weeks to months after infection, the fibrotic stage occurs. As a result of DAD, lung tissue fibrosis (lung scarring) takes place and causes long-term breathing difficulty. The epithelium lining the lungs is meant to be thin to allow oxygen to easily pass from alveoli to the bloodstream, but lung scarring thickens the membrane and compromises gas exchange. Long COVID is often marked by this scarring and irreversible damage to the alveoli, resulting in longlasting breathing and respiratory issues (Bösmüller et al.).

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The treatment for COVID-19 varies based on the severity of the infection. For mild cases, supportive care like hydration, rest, and antipyretics for fever is recommended. Severe cases often require hospitalization and may involve using oxygen therapy, antiviral medications like remdesivir, and corticosteroids like dexamethasone to reduce lung inflammation. In certain cases, monoclonal antibody therapies are administered to prevent disease progression in high-risk patients (Wiersinga et al., 2020). For critically ill patients, mechanical ventilation or extracorporeal membrane oxygenation (ECMO) may be necessary (Huang et al., 2021).

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There are two major classes of COVID-19 tests: diagnostic tests and antibody tests. A diagnostic test determines whether or an individual is currently infected with SARS-Cov-2, while an antibody test is used to determine if an individual has been infected in the past (FDA, 2022). Diagnostic tests can be either molecular or antigen tests. A molecular test uses polymerase chain reaction or another nucleic acid amplification test (NAAT) to detect the RNA produced by the virus. An antigen test (rapid test) detects antigens produced by the virus (FDA). A molecular test must be performed in a laboratory using a sample that is normally collected from the anterior nares using a swab. Samples can also be collected from the mid-turbinate, nasopharyngeal, or The sample can be collected at a testing center, in a doctor’s office, or at home using a kit. Results are not fast and take time to be processed. In contrast, antigen tests provide quick results and can be performed at home, but can be expired and inaccurate (FDA). COVID-19 antibody tests should not be performed to diagnose a patient, and they cannot ensure immunity to the virus. These tests require blood samples and tests for antibodies (B-cells)  the body has created against SARS-Cov-2 during a previous infection (FDA).

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During A COVID-19 infection, the host’s immune system produces antibodies that are specific to SARS-Cov-2. Multiple studies have shown that antibodies can be detected in the blood for up to a year after natural infection by the SARS-Cov-2 virus (Livieratos et al., 2024).  This provides a natural immunity, and while it does not eliminate the risk for infection, can lead to less severe symptoms in future infections. Vaccines have a similar affect as they introduce the virus in a small dose, allowing the immune system to produce antibodies. Whether an individual has natural immunity, vaccination, or both, it has been shown that there is 90% effectiveness in minimizing clinical severity in future infections (Livieratos et al.). When the host has natural or vaccine-derived immunity, the cytokine inflammatory response is milder resulting in milder symptoms. Additionally, the chances of developing COVID-pneomonia were drastically reduced after vaccination, and the chance of virus transmission was also decreased (Livieratos et al.). The new Omicron variant does show resistance to immunization, but hybrid immunity still shows evidence of protection against the variant. Vaccine boosters decreased susceptibility to the Omicron variant, and overall vaccinated individuals showed milder symptoms and fewer hospitalizations (Livieratos et al.). Overall, both natural and vaccine immunity provide protection against future infections from either the original SARS-Cov-2 virus or the omicron variant, and vaccines have been shown to play an important role in preventative measures.

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COVID-19 is primarily transmitted through respiratory droplets when an infected person coughs, sneezes, or talks. It can also spread via aerosols, particularly in poorly ventilated indoor spaces, and through contact with contaminated surfaces, although surface transmission is less common. Preventive measures include wearing masks, maintaining physical distancing, improving ventilation in indoor settings, practicing regular hand hygiene, and vaccinating to reduce the transmission and severity of the disease (Prather et al., 2020).