247 © 2024 The Author(s). Published by College of Education for Pure Science (Ibn Al-Haitham), University of Baghdad. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License Ibn Al-Haitham Journal for Pure and Applied Sciences Journal homepage: jih.uobaghdad.edu.iq PISSN: 1609-4042, EISSN: 2521-3407 IHJPAS. 2024, 37(4) Study the Effect of COVID-19 Disease on Thyroid Hormones (T3, T4, TSH) and the Lipid Profile in Recovering Iraqi Subjects Zainab Zouher Salman1,* , Sanad Baqer Mohammed2 and Samer Abdulhasan Muhi3 1,2Department of Chemistry, College of Sciences for Women, University of Baghdad, Baghdad, Iraq. 3Karkh Health Department, Al-Yarmouk Teaching Hospital, Baghdad, Iraq. *Corresponding Author. Received: 14 January 2023 Accepted: 14 March 2023 Published: 20 October 2024 doi.org/10.30526/37.4.3192 Abstract The present pandemic of Coronavirus Disease 2019 (COVID-19) causes many lasting impacts on the human body. It has immediate and extensive effects on the human body, particularly the thyroid gland. A rise in adenylyl cyclase 2 (ACE2) and transmembrane serine protease 2 (TMPRESS2) makes it easier for viruses to get into human cells. COVID-19 triggers a hyperactive immune response that produces interleukin-6 (IL-6) and other pro-inflammatory cytokines. This hyperactive immune response leads to severe thyroid malfunction. The current study aimed to research the relationship between the recovering Iraqi subjects of COVID-19 and thyroid hormones and lipid profiles. This study aims to evaluate triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH), and lipid profile including cholesterol, high-density lipoprotein (HDL), triglycerides (TG), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL). A total of 70 recovering subjects with COVID-19 were collected, and 50 were used as a control group. Thyroid hormones showed significant differences, an increase in serum TSH, and a decrease in the levels of T3 and T4 between the two groups (p= 0.001). The lipid profile revealed notable variations, as well as an increase in cholesterol, LDL, and VLDL. There was a notable drop in HDL levels between the two groups, as indicated through p-values of 0.001. Body mass index (BMI) and age did not show any significant differences. This research concludes that recovered people from COVID-19 had problems with their thyroid hormones and lipid profiles. Keywords: Lipid profile, recovered COVID -19, SARS-CoV-2, , thyroid hormones. 1. Introduction The 2019 coronavirus disease (COVID-19) is an extremely contagious virus that causes severe acute respiratory syndrome and has claimed the lives of more than 3.8 million people so far (SARS-CoV-2). It was in late 2019 when researchers in Wuhan, Central Province, China, first discovered SARS-CoV-2, a respiratory virus. It has now spread swiftly around the world. The Department of Health officially declared the pandemic on March 11, 2020. Since its declaration https://creativecommons.org/licenses/by/4.0/ https://creativecommons.org/licenses/by/4.0/ https://orcid.org/0000-0003-1057-9653 mailto:zainab.zouher1205a@csw.uobaghdad.edu.iq https://orcid.org/0000-0002-7377-2103 mailto:sanadala83@gmail.com https://orcid.org/0000-0003-2647-328X mailto:drsamermuhi@gmail.com IHJPAS. 2024, 37(4) 248 as a global pandemic, COVID-19 has wreaked havoc on healthcare systems in several countries. And then there's the epidemic [1]. Under an electron microscope, coronaviruses (CoVs) seem like crowns (in Latin, the word for "crown" is "corona.") because the membrane contains spike glycoproteins. The family Coronaviridae (order Nidovirales) includes the subfamily Orthocoronavirinae, which includes the four genera of CoVs: Alphacoronavirus, Betacoronavirus, Deltacoronavirus, and Gammacoronavirus (ɤ-CoV) [2,3]. Genomic evidence points to birds as the likely origin of gamma and delta coves, whereas bats and rodents are more likely to be the original hosts of α- and β- CoVs. CoVs almost always trigger outbreaks of respiratory diseases. Its diameter ranges from 60 to 140 nm, and it often has a pleomorphic form that is either round or elliptical. It is susceptible to heat and UV radiation, like other CoVs. This is true even though every viral species owes a debt to heat. SARS-CoV-2 deactivation temp studies are now underway [4,5]. It has been suspected that SARS-CoV-2, like SARS and MERS before it, spreads from bats to host species like pangolins and minks [6,7]. Multiple long-term effects on the human body's normal physiological balance have already been linked to the ongoing epidemic of COVID-19. Studies rapidly identified severe and complex impacts on human organ systems, including respiration, digestion, vascular, immune, renal, hepatic, cardiac, and hematological. In terms of the human endocrine system, COVID-19 studies are making slow but steady progress [8,9]. Hormones produced by the thyroid, including thyroxine (T4) and triiodothyronine (T3), play an important role in the brain and body from birth forward, including in cognitive and motor development [10,11]. The brain, heart, liver, and muscle all benefit from substances secreted by the thyroid gland. Thyroid stimulating hormone (TSH) is a hormone that is produced by the pituitary gland, which in turn is controlled by the hypothalamus secreting thyrotropin-releasing hormone (TRH), which in turn controls T3 and T4 synthesis [12-14]. This setup acts as a negative feedback loop. When T3 and T4 drop below normal, the pituitary gland releases TSH to stimulate the thyroid gland to make additional hormones and bring blood levels back up to normal. Once levels have risen, the pituitary gland will stop producing as much TSH. Thyroid hormones enter the circulation and distribute themselves accordingly. Although the majority of hormones are already coupled to proteins in the blood plasma, there are a few that may freely circulate in the circulation and potentially reach cells to drive metabolism [15,16]. With the publication of more studies on the effects of COVID-19 on the human thyroid, our understanding of the cause and treatment of thyroid dysfunction has improved. The thyroid glands produce more adenylate cyclase 2 (ACE2) and serine protease 2 transmembranes (TMPRESS2) than the lungs, and these two proteins work together to allow viruses to enter human cells [17,18]. COVID-19 triggers an overactive immune response that releases inflammatory cytokines, particularly interleukin-6 (IL-6), which modifies deiodinases and thyroid transport proteins, leading to obvious thyroid dysfunction. T3 levels fall as IL-6 concentrations rise, but TSH and T4 levels drop somewhat. This anomaly is characterized by the term "sick euthyroid syndrome" [19,20]. 2. Materials and Methods 2.1 Study subjects The current research was conducted in Iraq to study the effect of COVID-19 disease on thyroid hormones in recovered Iraqi subjects. This research included 120 individuals after getting patient permission and ethical clearance from the appropriate institutional review board. The subjects ranged in age from twenty to fifty-five years old. We collected 70 subjects with COVID-19 disease and 50 control subjects from Yarmouk Teaching Hospital and Mahmoudia General Hospital IHJPAS. 2024, 37(4) 249 between July 1, 2022, and September 1, 2022. Patients were classified into two groups: group 1 comprised 70 individuals (51 females and 19 males) recuperating from COVID-19; patients with a history of thyroid disease were excluded from the study, while group 2 comprised 50 individuals (37 females and 13 males) serving as the control group. 2.2 Blood sample collection Blood sample collection consisted of drawing five ml of venous blood and putting it in a blank tube at room temperature. Next, centrifuge it at 3000 r.p.m. for 10 minutes to extract the serum. We isolated the sera samples and stored them at -20 °C until we needed them. Serum was used to calculate (T3, T4, and TSH) by the ELISA technique and (cholesterol, TIR, and HDL). 2.3 Anthropometric Measurements Weight (kg) and height (cm): We calculated one's body mass index (BMI) (M2) by dividing one's weight (in kilograms) by one's height squared. 2.4 Characteristic of patients and control Patients with COVID-19 recovered. Disease and control were characterized by age, thyroid hormones, and lipid profile. 2.5 Statistical analysis The findings were all presented. as mean standard error (SE). The Statistical Package for the Social Sciences (SPSS), a computerized statistical tool for the social sciences was used for the analysis. A paired sample t-test was performed for the same group, including a comparison between the two groups. A p-value < 0.05 was considered to be statistically significant. 3. Results and Discussion The current study was arranged to evaluate some biochemical parameters in the serum samples of recovered subjects after post-infection COVID-19 and, apparently, the control group. Table 1 shows the mean ± SE of the age factor [(32.9 ± 1.2) (32.8 ± 1.6)] between recovered subjects and healthy controls, respectively, where the results presented non-significant variation between the two groups (p ≤ 0.05). While everyone is at risk of contracting COVID-19, those over the age of 65 are more vulnerable [21]. Table 1. Demographic factor distribution in studied groups. Parameters Groups Mean± SE p-value Age (Years) Recovered COVD19 subjects 32.90 ± 1.20 0.30 Control 32.80 ± 1.60 BMI (Kg/m2) Recovered COVD19 subjects 28.35 ± 1.00 0.06 Control 27.40 ± 0.70 two independent t-test were used at 0.05 α level Clinical symptoms appear in 21% (95% credible interval: 12-31%) of diseases in those ages 10 to 19, and 69% (57-82%) of infections in those over the age of 70. For those under the age of 20, the susceptibility to infection is almost half that of people over the age of 20 [22]. The result of the body mass index (BMI) is shown in Table 1. The results show that there was no significant difference between the two groups (p ≤ 0.05). The mean± SE for recovered patients was IHJPAS. 2024, 37(4) 250 16.51±0.530 and for healthy controls was 16.36±0.715. There is mounting evidence linking obesity to a more severe case of COVID-19 infection and an increased risk of death, according to many studies. After accounting for other factors, clinical research from China on the COVID-19 illness showed an 86% and 142% increased association between obesity and a severe infection compared to normal-weight people [23, 24]. It is necessary to obtain anthropometric data for COVID-19 patients, particularly the younger group, since obesity may have a crucial role in defining the severity of the disease. Future research should investigate the potential link between obesity and hospital mortality in COVID-19 patients [25]. Table 2. Comparison between recovered subjects and control in on thyroid hormones. Parameters Groups Mean± SE P-Value T3 recovered subjects 1.73± 0.05 0.001 healthy control 2.78± 0.07 T4 recovered subjects 310.31± 13.68 0.001 healthy control 684.17± 7.73 TSH recovered subjects 5.88± 0.22 0.001 healthy control 2.52± 0.10 Independent T-test were used at 0.05 α level. Table 2 shows that there are discernible differences between the groups for T3 level (1.73 ± 0.05) for the recovered patient group and (2.78 ± 0.07) for the healthy control group. The T3 values were significantly different between the two groups, with the recovered participants showing a lower T3 value than those in good health (p > 0.001). There are also significant differences between T4 levels (310.31 ± 13.68) for the recovered group and (684.17± 7.73) for the healthy group control. In the mean T4, there were significant differences. There was a decrease in the T4 value in the recovered group (p > 0.001). Also, there are big differences between TSH levels (5.88 ± 0.22) for the recovered group and (2.52 ± 0.10) for those in good health. The median TSH levels varied significantly. There was an increase in the TSH value in the recovered group (p > 0.001). Serum levels of T3, T4, and TSH in SARS were shown to be significantly different from those in controls during the progression and recovery phases [26]. The current data revealed that TSH levels were significantly higher in COVID-19 patients who were moderately or severely affected, compared to those who were not [19]. Patients with COVID-19 also had significantly higher TT3 increases than those without the disease, but TT4 levels changed very little [19]. The TSH, fT4, and fT3 levels of another study done 3 months after infection were all within the usual range. It has been observed no significant difference in TSH and FT4 levels from pre-COVID-19 baseline levels and a restoration of individual autonomic set points for fT4 and TSH [27]. In a study conducted in Iraq among individuals infected with COVID-19, blood levels of both TSH and T3 were significantly lower compared to levels of a healthy control group [28]. IHJPAS. 2024, 37(4) 251 Table 3. Comparison between recovered subjects and control in lipid profile. Parameters Groups Mean± SE p-Value Cholesterol recovered subjects 219.287± 1.009 0.001 healthy control 184.85± 1.009 TG recovered subjects 215.995± 1.063 0.001 healthy control 189.716± 1.935 HDL recovered subjects 29.396± 0.45 0.001 healthy control 84.617± 2.061 LDL recovered subjects 146.692± 0.899 0.001 healthy control 62.289± 2.268 VLDL recovered subjects 43.199± 0.212 0.001 healthy control 37.943± 0.387 Independent T-test were used at 0.05 α level. Table 3 demonstrates that there are discernible differences in cholesterol level between the groups, with (219.287± 1.009) for the recovered patient group and (184.85± 1.009) for the healthy control group. Cholesterol values were significantly different between the two groups, with the recovered participants showing an increased cholesterol value than those in good health (p > 0.001). Also, significant differences were found between the two groups with regard to TG level (215.995 ±1.063) for the recovered patient group and (189.716±1.935) for the healthy control group. TG values were significantly different between the two groups, with the recovered participants showing an increased TG value than those in good health (p > 0.001). The serum HDL level was significant between the two groups (29.396±0.45) for the recovered patient group and (84.617±2.061) for the healthy control group. HDL values were significantly different between the two groups, with recovered participants showing a lower HDL value than those in good health (p > 0.001). Additionally, a significant increase in TSH levels was observed in the recovered group, which set them apart from the control group (p > 0.001). The level of VLDL also showed significant differences (43.199 ± 0.212) for the recovered patient group and (37.943±0.387) for the healthy control group. Between the two groups, HDL values were different, with recovered participants showing a lower HDL value than healthy subjects (p > 0.001). Lipid metabolism of recovered individuals has been investigated many years after they had contracted SARS. They discovered that the levels of TG and cholesterol were substantially higher than in people who had recovered [29]. Statistics revealed substantial differences between the recovered subjects and the healthy controls. Triglycerides were significantly higher following recovery compared to the infection's acute phase (p= 0.0001) [30]. Statistically significant changes were found when comparing the recovered subjects with healthy controls. Compared to the acute phase of the infection, HDL cholesterol, LDL cholesterol, and TG were considerably higher after recovery (p= 0.0001) [30]. Moreover, 12 years after contracting SARS, researchers studied the lipid metabolism of recovered patients and found that TG, VLDL, and cholesterol readings were significantly higher than in recovered participants [29]. IHJPAS. 2024, 37(4) 252 4. Conclusion The study's results show that some biochemical parameters are important. For example, serum levels of TSH, cholesterol, TG, LDL, and VLDL increased, while levels of T3, T4, and HDL decreased (p > 0.05) in the recovered subjects compared to the control group. Acknowledgment The authors thank the Department of Chemistry, College of Science for Women, University of Baghdad for research approval. Conflict of Interest The authors declare that they have no conflicts of interest. Funding No founding. Ethical Clearance The University of Baghdad's local Ethical Committee approved the project. The Medical Research Ethics Committee of the Ministry of Health, Baghdad Health Department, Al-Karkh, Baghdad, Iraq, approved the research (No. 39563 on 27/7/2022). References 1. Jasim, R.Z. Biochemical Action of Vaccines in Iraqi Patients with COVID-19 Infection. Baghdad Science Journal 2023, 20(4 (SI)), 1469-1479. https://doi.org/10.21123/bsj.2023.8750. 2. Parlikar, A.; Kalia, K.; Sinha, S.; Patnaik, S.; Sharma, N.; Vemuri, S.G.; Sharma, G. Understanding Genomic Diversity, Pan-Genome, and Evolution of SARS-Cov-2. Peer J 2020, 8, e9576. https://doi.org/10.7717/peerj.9576. 3. Balasuriya, U.B.; Go, Y.Y.; Carossino, M. Coronaviridae and Tobaniviridae, 4th ed. Veterinary Microbiology, John Wiley & Sons, Inc. 2022, Ch. 61, pp. 622-658. https://doi.org/10.1002/9781119650836.ch61. 4. Biryukov, J.; Boydston, J.A.; Dunning, R.A.; Yeager, J.J.; Wood, S.; Ferris, A.; Miller, D.; Weaver, W.; Zeitouni, N.E.; Freeburger, D. SARS-Cov-2 is Rapidly Inactivated at High Temperature. Environmental Chemistry Letters 2021, 19(2), 1773–1777. https://doi.org/10.1007/s10311-021- 01187-x. 5. Chin, A.W.H.; Chu, J.T.S.; Perera, M.R.A.; Hui, K.P.Y.; Yen, H.L.; Chan, M.C.W.; Peiris, M.; Poon, L.L.M. Stability of SARS-CoV-2 in Different Environmental Conditions. Lancet Microbe 2020, 1(1), e10. https://doi.org/10.1016/S2666-5247(20)30003-3. 6. Zhang, T.; Wu, Q.; Zhang, Z. Probable Pangolin Origin of SARS-Cov-2 Associated with the COVID- 19 Outbreak. Current Biology:CB 2020, 30(7), 1346–1351. https://doi.org/10.1016/j.cub.2020.03.022 . 7. Hossain, M.G.; Javed, A.; Akter, S.; Saha, S. SARS-CoV-2 Host Diversity: An Update of Natural Infections and Experimental Evidence. Journal of Microbiology, Immunology and Infection 2021, 54(2), 175-181. https://doi.org/10.1016/j.jmii.2020.06.006. 8. Scappaticcio, L.; Pitoia, F.; Esposito, K.; Piccardo, A.; Trimboli, P. Impact of COVID-19 on the Thyroid Gland: An Update. Reviews in Endocrine and Metabolic Disorders 2021, 22(4), 803–815. https://doi.org/10.1007/s11154-020-09615-z. 9. Jain, U. Effect of COVID-19 on the Organs. Cureus 2020, 12(8), e9540. https://doi.org/ 10.7759/cureus.9540. https://doi.org/10.21123/bsj.2023.8750 https://doi.org/10.7717/peerj.9576 https://doi.org/10.1002/9781119650836.ch61 https://doi.org/10.1007/s10311-021-01187-x https://doi.org/10.1007/s10311-021-01187-x https://doi.org/10.1016/S2666-5247(20)30003-3 https://doi.org/10.1016/j.cub.2020.03.022 https://doi.org/10.1016/j.jmii.2020.06.006 https://doi.org/10.7759%2Fcureus.9540 IHJPAS. 2024, 37(4) 253 10. Gilbert, M.E.; O’Shaughnessy, K.L.; Axelstad, M. Regulation of Thyroid-Disrupting Chemicals to Protect the Developing Brain. Endocrinology 2020, 161(10), bqaa106. https://doi.org/10.1210/endocr/bqaa106. 11. Grossklaus, R.; Liesenkötter, K.P.; Doubek, K.; Völzke, H.; Gaertner, R. Iodine Deficiency, Maternal Hypothyroxinemia and Endocrine Disrupters Affecting Fetal Brain Development: A Scoping Review. Nutrients 2023, 15(10), 2249. https://doi.org/10.3390/nu15102249. 12. Crawford, A.; Harris, H. Tipping The Scales: Understanding Thyroid Imbalances. Nursing 2020 Critical Care 2013, 8(1), 23–28. https://doi.org/ 10.1097/01.CCN.0000418818.21604.22. 13. Hershman, J.M.; Beck-Peccoz, P. Discoveries Around the Hypothalamic–Pituitary–Thyroid Axis. Thyroid 2023, 33(7), 785-790. https://doi.org/10.1089/thy.2022.0258. 14. Giannocco, G.; Kizys, M.M.L.; Maciel, R.M.; de Souza, J.S. Thyroid Hormone, Gene Expression, and Central Nervous System: Where We Are. Seminars in Cell & Developmental Biology 2021, 114, 47-56. Academic Press. https://doi.org/10.1016/j.semcdb.2020.09.007. 15. Mohiuddin, A.K. Clinical Pharmacists in Chronic Care [Part 2]. Archives in Biomedical Engineering & Biotechnology 2020, 3(4), 1-41. https://doi.org/ 10.33552/ABEB.2019.03.000566. 16. Mendez, D.A.; Soñanez-Organis, J.G.; Yang, X.; Vazquez-Anaya, G.; Nishiyama, A.; Ortiz, R.M. Exogenous Thyroxine Increases Cardiac GLUT4 Translocation in Insulin Resistant OLETF Rats. Molecular and Cellular Endocrinology 2024, 590, 112254. https://doi.org/10.1016/j.mce.2024.112254. 17. Barrea, L.; Caprio, M.; Grassi, D.; Cicero, A.F.G.; Bagnato, C.; Paolini, B.; Muscogiuri, G.A. New Nomenclature for the Very Low-Calorie Ketogenic Diet (VLCKD): Very Low-Energy Ketogenic Therapy (VLEKT). Ketodiets and Nutraceuticals Expert Panels:“KetoNut”, Italian Society of Nutraceuticals (SINut) and the Italian Association of Dietetics and Clinical Nutrition (ADI). Current Nutrition Reports 2024, 13(3), 552-556. https://doi.org/10.1007/s13668-024-00560-w. 18. Tagliabue, A.; Armeno, M.; Berk, K.A.; Guglielmetti, M.; Ferraris, C.; Olieman, J.; Van der Louw, E. Ketogenic Diet for Epilepsy and Obesity: Is It The Same?. Nutrition, Metabolism and Cardiovascular Diseases 2024, 34(3), 581-589. https://doi.org/10.1016/j.numecd.2024.01.014. 19. Malik, J.; Malik, A.; Javaid, M.; Zahid, T.; Ishaq, U.; Shoaib, M. Thyroid Function Analysis in COVID- 19: A Retrospective Study from A Single Center. PLOS One 2021, 16(3), e0249421. https://doi.org/10.1371/journal.pone.0249421. 20. Parihar, A.; Malviya, S.; Khan, R.; Kaushik, A.; Mostafavi, E. COVID-19 Associated Thyroid Dysfunction and Other Comorbidities and its Management Using Phytochemical-Based Therapeutics: A Natural Way. Bioscience Reports 2023, 43(7), BSR20230293. https://doi.org/10.1042/BSR20230293. 21. Haldar, A.; Sethi, N. The Effect of Country-Level Factors and Government Intervention on the Incidence Of COVID-19. Asian Economics Letters 2020, 1(2), 17804. https://doi.org/10.46557/001c.17804. 22. Davies, N.G.; Klepac, P.; Liu, Y.; Prem, K.; Jit, M.; Eggo, R.M. Age-Dependent Effects in the Transmission and Control of COVID-19 Epidemics. Nature Medicine 2020, 26(8), 1205–1211 https://doi.org/10.1038/s41591-020-0962-9. 23. Shah, H.; Khan, M.S.H.; Dhurandhar, N. V; Hegde, V. The Triumvirate: Why Hypertension, Obesity, and Diabetes are Risk Factors for Adverse Effects in Patients with COVID-19. Acta Diabetologica 2021, 58(7), 831–843. https://doi.org/10.1007/s00592-020-01636-z. 24. Chu, Y.; Yang, J.; Shi, J.; Zhang, P.; Wang, X. Obesity is Associated with Increased Severity of Disease in COVID-19 Pneumonia: A Systematic Review and Meta-Analysis. European Journal of Medical Research 2020, 25(1), 1–15. https://doi.org/10.1186/s40001-020-00464-9. 25. Chen, M.; Zhou, W.; Xu, W. Thyroid Function Analysis in 50 Patients with COVID-19: A Retrospective Study. Thyroid 2021, 31(1), 8–11. https://doi.org/10.1089/thy.2020.0363. 26. Clarke, S.A.; Phylactou, M.; Patel, B.; Mills, E.G.; Muzi, B.; Izzi-Engbeaya, C.; Choudhury, S.; Khoo, B.; Meeran, K.; Comninos, A.N. Normal Adrenal and Thyroid Function in Patients Who Survive https://doi.org/10.1210/endocr/bqaa106 https://doi.org/10.3390/nu15102249 https://doi.org/10.1089/thy.2022.0258 https://doi.org/10.1016/j.semcdb.2020.09.007 https://doi.org/10.1016/j.mce.2024.112254 https://doi.org/10.1016/j.numecd.2024.01.014 https://doi.org/10.1371/journal.pone.0249421 https://doi.org/10.1042/BSR20230293 https://doi.org/10.46557/001c.17804 https://doi.org/10.1089/thy.2020.0363 IHJPAS. 2024, 37(4) 254 COVID-19 Infection. The Journal of Clinical Endocrinology and Metabolism 2021, 106(8), 2208– 2220. https://doi.org/10.1210/clinem/dgab349. 27. Mohammed, A.H.; Yousif, A.M.; Jabbar, S.A.; Ismail, P.A. Assessment of Thyroid Function in COVID-19 Patients. Tabari Biomedical Student Research Journal 2021, 3(3), 8-13. https://doi.org/10.18502/tbsrj.v3i3.6930. 28. Pecon-Slattery, J. Recent Advances in Primate Phylogenomics. Annual Review of Animal Biosciences 2014, 2, 41-63. https://doi.org/10.1146/annurev-animal-022513-114217. 29. Roccaforte, V.; Daves, M.; Lippi, G.; Spreafico, M.; Bonato, C. Altered Lipid Profile in Patients with COVID-19 Infection. Journal of Laboratory and Precision 2021, 6(2), 1-8. https://doi.org/10.21037/jlpm-20-98. 30. Taha, E.M.; Al-Taweil, H.I.; Noura, K.M.S.; Yusoff, W.M.W.; Omar, O.; Hamid, A.A. Biochemical Characterization for Lipid Synthesis in Aspergillus niger. Baghdad Science Journal 2016, 13(2.2 NCC), 0375-0375. https://doi.org/10.21123/bsj.2016.13.2.2NCC.0375. https://doi.org/10.1210/clinem/dgab349 https://doi.org/10.18502/tbsrj.v3i3.6930 https://doi.org/10.18502/tbsrj.v3i3.6930 https://pubmed.ncbi.nlm.nih.gov/25384134/ https://doi.org/10.1146/annurev-animal-022513-114217 https://doi.org/10.21123/bsj.2016.13.2.2NCC.0375