International Journal of Clinical and Experimental Medical Sciences

| Peer-Reviewed |

Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19

Received: 16 August 2021    Accepted: 07 September 2021    Published: 27 September 2021
Views:       Downloads:

Share This Article

Abstract

This article highlights main aspects of pathogenesis of age-related macular degeneration (AMD) and the connection between SARS-CoV-2 and diseases of the posterior pole of the eyes. Background: A novel coronavirus disease COVID-19 is actual nowadays due to its multiple organ damage, including eye tissues. Retina is also a target organ. AMD is the most common cause of central vision loss and its development is connected not only with ageing, but also with some other factors. Last years ophthalmological community considers virus infection to be a predictor and trigger for developing of AMD. Objective: Several theories have been proposed for the development of AMD. The most common theories are vascular due to pathogenetically significant decrease in blood flow in the pool of the carotid arteries; metabolic disorders (systemic and local); oxidative stress in endothelial cells; hereditary predisposition. Inflammation as a pathogenetic mechanism appeared in a novel light of discoveries in developing of not only AMD, but also some other eye diseases. The connection between SARS-CoV-2 and diseases of the posterior pole known nowadays are conjunctivitis, central retinal vein occlusion, isolated inflammatory optic neuritis, acute bilateral demyelinating optic neuritis. Thus, the question is still open. Conclusion: no single theory of the development of AMD can absolutely explain the diversity of pathological changes in of the retina and choroid tissues. Further study of the role of each factor of pathogenesis– from molecular to tissue will allow the development of fundamentally novel and perspective directions of AMD therapy.

DOI 10.11648/j.ijcems.20210705.11
Published in International Journal of Clinical and Experimental Medical Sciences (Volume 7, Issue 5, September 2021)
Page(s) 127-137
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Age-related Macular Degeneration, COVID-19, Virus Infection

References
[1] Flaxel, C., Adelman, R., Bailey, S., Fawzi, A., Lim, J., Vemulakonda, G., & Ying, G. (2020). Age-Related Macular Degeneration Preferred Practice Pattern®. Ophthalmology, 127 (1), P1-P65.
[2] Budzinskaja M. V., Gurova I. V. (2006). Subretinal neovascular membrane in age-related macular degeneration. Vestnik oftal'mologii, 122 (4): 49–54.
[3] Izmajlov A. S. (2001). Choroidal neovascularization. Sankt-Petersburg: SPbMAPO.
[4] Cruickshanks, K. (1997). The Prevalence of Age-Related Maculopathy by Geographic Region and Ethnicity. Archives Of Ophthalmology, 115 (2), 242.
[5] Tomany, S., Wang, J., van Leeuwen, R., Klein, R., Mitchell, P., & Vingerling, J. et al. (2004). Risk factors for incident age-related macular degeneration. Ophthalmology, 111 (7), 1280-1287.
[6] Seddon, J., Ajani, U., & Mitchell, B. (1997). Familial Aggregation of Age-related Maculopathy. American Journal Of Ophthalmology, 123 (2), 199-206.
[7] Bikbov M. M., Fajzrahmanov R. R., Jarmukhametova A. L. (2013). Age related macular degeneration. Moscow: Aprel'; 2013.
[8] Gvetadze A. A., Koroleva I. A. Age-related macular degeneration. Modern look at the issiue. Review. Rossijskij Meditsinskij Zhurnal. Klinicheskaja oftal'mologija, 1: 37–41.
[9] Ryzhova L. S. (1991). The hemodynamics of the brain and eye in patients with presenile and senile nonexudative central chorioretinal dystrophy during health resort treatment. Vestnik oftal'mologii, 7 (6): 21–3.
[10] Vincent GK, Velkoff VA. The next four decades, the older population in the United States: 2010 to 2050. 2010; P25-1138. Available at: www.census.gov/prod/2010pubs/p25-1138.pdf. Accessed August 2021.
[11] Vit V. V. (2003). The structure of the human visual system. Odessa: Astroprint.
[12] Panova I. E., Prokop'eva M. Ju., Kinzerskij A. Ju., Sadretdinova E. R. (2007). Status of local hemodynamics in the initial stage of age-related macular degeneration. Kataraktal'naja i refrakcionnaja khirurgija, 7 (4): 32–6.
[13] Ramrattan, R. S., van der Schaft, T. L., Mooy, C. M., de Bruijn, W. C., Mulder, P. G., & de Jong, P. T. (1994). Morphometric analysis of Bruch's membrane, the choriocapillaris, and the choroid in aging. Investigative ophthalmology & visual science, 35 (6), 2857–2864.
[14] Prokop'eva M. Ju., Panova I. E., Kinzerskij A. Ju., Ermak E. M., Tonkikh N. A. (2006). Features of local blood flow in various forms of age-related macular degeneration. Vestnik Orenburgskogo gosudarstvennogo universiteta, S11 (61): 235–7.
[15] Kiseleva T. N. (2004). Ul'trazvukovye metody issledovaniia krovotoka v diagnostike ishemicheskikh porazheniĭ glaza. Vestnik oftalmologii, 120 (4), 3–5.
[16] Krasnov M. M., Kuznetsova I. I. Ultrasonic dopplerography in the diagnosis of vascular eye diseases. Vestnik oftal'mologii. 1981; 97 (6): 26–7.
[17] Klettner, A., Kauppinen, A., Blasiak, J., Roider, J., Salminen, A., & Kaarniranta, K. (2013). Cellular and molecular mechanisms of age-related macular degeneration: from impaired autophagy to neovascularization. The international journal of biochemistry & cell biology, 45 (7), 1457–1467.
[18] Gvarishvili E. P. (1999). Using of pharmacological and physical treatment in the therapy of chorioretinal dystrophies: cand. dis. of med. sci. Moscow.
[19] Abdullaeva E. A. (2002). Pathogenetic therapy of central involute chorioretinal dystrophy: cand. dis. of med. sci. Ufa.
[20] Panormova N. V. (1983). Choroidal microcirculation in general vascular pathology. Morfologicheskie aspekty oftal'mologii.
[21] Baranov V. I., Golikov B. M. State of retinal hemodynamics in patients with primary arterial hypotension. Vestnik oftal'mologii, 1984; 100 (2): 50–3.
[22] Selitskaja T. I. (1977), Age-related macular degeneration and atherosclerosis. Oftal'mologicheskij zhurnal, 1: 50–2.
[23] Curcio, C. A., Johnson, M., Huang, J. D., & Rudolf, M. (2009). Aging, age-related macular degeneration, and the response-to-retention of apolipoprotein B-containing lipoproteins. Progress in retinal and eye research, 28 (6), 393–422.
[24] Olofsson, S. O., & Borèn, J. (2005). Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. Journal of internal medicine, 258 (5), 395–410.
[25] Beatty, S., Koh, H., Phil, M., Henson, D., & Boulton, M. (2000). The role of oxidative stress in the pathogenesis of age-related macular degeneration. Survey of ophthalmology, 45 (2), 115–134.
[26] Drobek-Słowik, M., Karczewicz, D., & Safranow, K. (2007). Potencjalny udział stresu oksydacyjnego w patogenezie zwyrodnienia plamki zwiazanego z wiekiem (AMD) [The potential role of oxidative stress in the pathogenesis of the age-related macular degeneration (AMD)]. Postepy higieny i medycyny doswiadczalnej (Online), 61, 28–37.
[27] Yildirim, Z., Ucgun, N. I., & Yildirim, F. (2011). The role of oxidative stress and antioxidants in the pathogenesis of age-related macular degeneration. Clinics (Sao Paulo, Brazil), 66 (5), 743–746.
[28] Kaneto, H., Katakami, N., Matsuhisa, M., & Matsuoka, T. A. (2010). Role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis. Mediators of inflammation, 2010, 453892.
[29] Rodrigo, R., González, J., & Paoletto, F. (2011). The role of oxidative stress in the pathophysiology of hypertension. Hypertension research: official journal of the Japanese Society of Hypertension, 34 (4), 431–440.
[30] Davies K. J. (1995). Oxidative stress: the paradox of aerobic life. Biochemical Society symposium, 61, 1–31.
[31] Rattan S. I. (2006). Theories of biological aging: genes, proteins, and free radicals. Free radical research, 40 (12), 1230–1238.
[32] Valko, M., Leibfritz, D., Moncol, J., Cronin, M. T., Mazur, M., & Telser, J. (2007). Free radicals and antioxidants in normal physiological functions and human disease. The international journal of biochemistry & cell biology, 39 (1), 44–84.
[33] Hageman, G. S., Luthert, P. J., Victor Chong, N. H., Johnson, L. V., Anderson, D. H., & Mullins, R. F. (2001). An integrated hypothesis that considers drusen as biomarkers of immune-mediated processes at the RPE-Bruch's membrane interface in aging and age-related macular degeneration. Progress in retinal and eye research, 20 (6), 705–732.
[34] Medeiros, N. E., & Curcio, C. A. (2001). Preservation of ganglion cell layer neurons in age-related macular degeneration. Investigative ophthalmology & visual science, 42 (3), 795–803.
[35] Haimovici, R., Gantz, D. L., Rumelt, S., Freddo, T. F., & Small, D. M. (2001). The lipid composition of drusen, Bruch's membrane, and sclera by hot stage polarizing light microscopy. Investigative ophthalmology & visual science, 42 (7), 1592–1599.
[36] Sparrow, J. R., Kim, S. R., & Wu, Y. (2010). Experimental approaches to the study of A2E, a bisretinoid lipofuscin chromophore of retinal pigment epithelium. Methods in molecular biology (Clifton, N. J.), 652, 315–327.
[37] Eldred, G. E., & Lasky, M. R. (1993). Retinal age pigments generated by self-assembling lysosomotropic detergents. Nature, 361 (6414), 724–726.
[38] Finnemann, S. C., Leung, L. W., & Rodriguez-Boulan, E. (2002). The lipofuscin component A2E selectively inhibits phagolysosomal degradation of photoreceptor phospholipid by the retinal pigment epithelium. Proceedings of the National Academy of Sciences of the United States of America, 99 (6), 3842–3847.
[39] Suter, M., Remé, C., Grimm, C., Wenzel, A., Jäättela, M., Esser, P., Kociok, N., Leist, M., & Richter, C. (2000). Age-related macular degeneration. The lipofusion component N-retinyl-N-retinylidene ethanolamine detaches proapoptotic proteins from mitochondria and induces apoptosis in mammalian retinal pigment epithelial cells. The Journal of biological chemistry, 275 (50), 39625–39630.
[40] Kannan, R., Zhang, N., Sreekumar, P. G., Spee, C. K., Rodriguez, A., Barron, E., & Hinton, D. R. (2006). Stimulation of apical and basolateral VEGF-A and VEGF-C secretion by oxidative stress in polarized retinal pigment epithelial cells. Molecular vision, 12, 1649–1659.
[41] Klettner, A., & Roider, J. (2009). Constitutive and oxidative-stress-induced expression of VEGF in the RPE are differently regulated by different Mitogen-activated protein kinases. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 247 (11), 1487–1492.
[42] Wu, W. C., Hu, D. N., Gao, H. X., Chen, M., Wang, D., Rosen, R., & McCormick, S. A. (2010). Subtoxic levels hydrogen peroxide-induced production of interleukin-6 by retinal pigment epithelial cells. Molecular vision, 16, 1864–1873.
[43] Penn, J. S., Madan, A., Caldwell, R. B., Bartoli, M., Caldwell, R. W., & Hartnett, M. E. (2008). Vascular endothelial growth factor in eye disease. Progress in retinal and eye research, 27 (4), 331–371.
[44] Boĭko, É. V., Churashov, S. V., & Kamilova, T. A. (2013). Vestnik oftalmologii, 129 (2), 86–90.
[45] Byeon, S. H., Lee, S. C., Choi, S. H., Lee, H. K., Lee, J. H., Chu, Y. K., & Kwon, O. W. (2010). Vascular endothelial growth factor as an autocrine survival factor for retinal pigment epithelial cells under oxidative stress via the VEGF-R2/PI3K/Akt. Investigative ophthalmology & visual science, 51 (2), 1190–1197.
[46] Hammond, C. J., Webster, A. R., Snieder, H., Bird, A. C., Gilbert, C. E., & Spector, T. D. (2002). Genetic influence on early age-related maculopathy: a twin study. Ophthalmology, 109 (4), 730–736.
[47] Silvestri, G., Johnston, P. B., & Hughes, A. E. (1994). Is genetic predisposition an important risk factor in age-related macular degeneration? Eye (London, England), 8 (Pt 5), 564–568.
[48] Seddon, J. M., Cote, J., Page, W. F., Aggen, S. H., & Neale, M. C. (2005). The US twin study of age-related macular degeneration: relative roles of genetic and environmental influences. Archives of ophthalmology (Chicago, Ill.: 1960), 123 (3), 321–327.
[49] Hageman, G. S., Anderson, D. H., Johnson, L. V., Hancox, L. S., Taiber, A. J., Hardisty, L. I., Hageman, J. L., Stockman, H. A., Borchardt, J. D., Gehrs, K. M., Smith, R. J., Silvestri, G., Russell, S. R., Klaver, C. C., Barbazetto, I., Chang, S., Yannuzzi, L. A., Barile, G. R., Merriam, J. C., Smith, R. T., … Allikmets, R. (2005). A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proceedings of the National Academy of Sciences of the United States of America, 102 (20), 7227–7232.
[50] Rabson, A., Rabson, A., & Delves, P. (2005). Really essential medical immunology. Blackwell Publishing.
[51] Zareparsi, S., Branham, K. E., Li, M., Shah, S., Klein, R. J., Ott, J., Hoh, J., Abecasis, G. R., & Swaroop, A. (2005). Strong association of the Y402H variant in complement factor H at 1q32 with susceptibility to age-related macular degeneration. American journal of human genetics, 77 (1), 149–153.
[52] Johnson, P. T., Betts, K. E., Radeke, M. J., Hageman, G. S., Anderson, D. H., & Johnson, L. V. (2006). Individuals homozygous for the age-related macular degeneration risk-conferring variant of complement factor H have elevated levels of CRP in the choroid. Proceedings of the National Academy of Sciences of the United States of America, 103 (46), 17456–17461.
[53] Penfold, P. L., Killingsworth, M. C., & Sarks, S. H. (1985). Senile macular degeneration: the involvement of immunocompetent cells. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 223 (2), 69–76.
[54] Zeng, F., Zhang, M., Xu, Y., & Xu, H. (2013). ARMS2 interference leads to decrease of proinflammatory mediators. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 251 (11), 2539–2544.
[55] Hooks, J. J., Chan, C. C., & Detrick, B. (1988). Identification of the lymphokines, interferon-gamma and interleukin-2, in inflammatory eye diseases. Investigative ophthalmology & visual science, 29 (9), 1444–1451.
[56] Cousins, S. W., Espinosa-Heidmann, D. G., & Csaky, K. G. (2004). Monocyte activation in patients with age-related macular degeneration: a biomarker of risk for choroidal neovascularization? Archives of ophthalmology (Chicago, Ill.: 1960), 122 (7), 1013–1018.
[57] Kutty R. K., Nagineni C. N., Samuel W., et al. Differential regulation of microRNA-146a and microRNA-146b-5p in human retinal pigment epithelial cells by interleukin-1β, tumor necrosis factor-α, and interferon-γ. Molecular vision. 2013; 19: 737–50
[58] Ketlinskij S. A., Simbircev A. S. (2008). Cytokines. Sankt-Petersburg: Foliant.
[59] Ozaki, E., Campbell, M., & Doyle, S. L. (2015). Targeting the NLRP3 inflammasome in chronic inflammatory diseases: current perspectives. Journal of inflammation research, 8, 15–27.
[60] Doyle, S. L., Campbell, M., Ozaki, E., Salomon, R. G., Mori, A., Kenna, P. F., Farrar, G. J., Kiang, A. S., Humphries, M. M., Lavelle, E. C., O'Neill, L. A., Hollyfield, J. G., & Humphries, P. (2012). NLRP3 has a protective role in age-related macular degeneration through the induction of IL-18 by drusen components. Nature medicine, 18 (5), 791–798.
[61] Kauppinen, A., Niskanen, H., Suuronen, T., Kinnunen, K., Salminen, A., & Kaarniranta, K. (2012). Oxidative stress activates NLRP3 inflammasomes in ARPE-19 cells--implications for age-related macular degeneration (AMD). Immunology letters, 147 (1-2), 29–33.
[62] Tarallo, V., Hirano, Y., Gelfand, B. D., Dridi, S., Kerur, N., Kim, Y., Cho, W. G., Kaneko, H., Fowler, B. J., Bogdanovich, S., Albuquerque, R. J., Hauswirth, W. W., Chiodo, V. A., Kugel, J. F., Goodrich, J. A., Ponicsan, S. L., Chaudhuri, G., Murphy, M. P., Dunaief, J. L., Ambati, B. K., … Ambati, J. (2012). DICER1 loss and Alu RNA induce age-related macular degeneration via the NLRP3 inflammasome and MyD88. Cell, 149 (4), 847–859.
[63] Watanabe, K., Zhang, X. Y., Kitagawa, K., Yunoki, T., & Hayashi, A. (2009). The effect of clonidine on VEGF expression in human retinal pigment epithelial cells (ARPE-19). Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 247 (2), 207–213.
[64] Nagineni, C. N., Kommineni, V. K., William, A., Detrick, B., & Hooks, J. J. (2012). Regulation of VEGF expression in human retinal cells by cytokines: implications for the role of inflammation in age-related macular degeneration. Journal of cellular physiology, 227 (1), 116–126.
[65] Jonas, J. B., Tao, Y., Neumaier, M., & Findeisen, P. (2010). Monocyte chemoattractant protein 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 in exudative age-related macular degeneration. Archives of ophthalmology (Chicago, Ill.: 1960), 128 (10), 1281–1286.
[66] Huang, H., Parlier, R., Shen, J. K., Lutty, G. A., & Vinores, S. A. (2013). VEGF receptor blockade markedly reduces retinal microglia/macrophage infiltration into laser-induced CNV. PloS one, 8 (8), e71808.
[67] Hahn, G., Jores, R., & Mocarski, E. S. (1998). Cytomegalovirus remains latent in a common precursor of dendritic and myeloid cells. Proceedings of the National Academy of Sciences of the United States of America, 95 (7), 3937–3942.
[68] Slobedman, B., Mocarski, E. S., Arvin, A. M., Mellins, E. D., & Abendroth, A. (2002). Latent cytomegalovirus down-regulates major histocompatibility complex class II expression on myeloid progenitors. Blood, 100 (8), 2867–2873.
[69] Cinatl, J., Jr, Vogel, J. U., Kotchetkov, R., Scholz, M., & Doerr, H. W. (1999). Proinflammatory potential of cytomegalovirus infection. specific inhibition of cytomegalovirus immediate-early expression in combination with antioxidants as a novel treatment strategy?. Intervirology, 42 (5-6), 419–424.
[70] Espinosa-Heidmann, D. G., Suner, I. J., Hernandez, E. P., Monroy, D., Csaky, K. G., & Cousins, S. W. (2003). Macrophage depletion diminishes lesion size and severity in experimental choroidal neovascularization. Investigative ophthalmology & visual science, 44 (8), 3586–3592.
[71] Fabricant, C. G., Krook, L., & Gillespie, J. H. (1973). Virus-induced cholesterol crystals. Science (New York, N. Y.), 181 (4099), 566–567.
[72] Baranova E. G., Parkhomenko Ju. V., Sizikova O. N., Ivanov P. A., Krasnoperov V. G. (2006). Comparative analysis of total coronary lesions, dyslipidemia and the fact of infection with herpes simplex virus 1, 2 types, cytomegalovirus in patients with coronary heart disease. Dal'nevostochnyj medicinskij zhurnal, 4: 5–7.
[73] Benditt, E. P., Barrett, T., & McDougall, J. K. (1983). Viruses in the etiology of atherosclerosis. Proceedings of the National Academy of Sciences of the United States of America, 80 (20), 6386–6389.
[74] Fabricant, C. G., Fabricant, J., Litrenta, M. M., & Minick, C. R. (1978). Virus-induced atherosclerosis. The Journal of experimental medicine, 148 (1), 335–340.
[75] Miller, D. M., Espinosa-Heidmann, D. G., Legra, J., Dubovy, S. R., Sũner, I. J., Sedmak, D. D., Dix, R. D., & Cousins, S. W. (2004). The association of prior cytomegalovirus infection with neovascular age-related macular degeneration. American journal of ophthalmology, 138 (3), 323–328.
[76] Cannon, M. J., Schmid, D. S., & Hyde, T. B. (2010). Review of cytomegalovirus seroprevalence and demographic characteristics associated with infection. Reviews in medical virology, 20 (4), 202–213.
[77] Griffiths, P., Baraniak, I., & Reeves, M. (2015). The pathogenesis of human cytomegalovirus. The Journal of pathology, 235 (2), 288–297.
[78] Jarvis, M. A., & Nelson, J. A. (2007). Human cytomegalovirus tropism for endothelial cells: not all endothelial cells are created equal. Journal of virology, 81 (5), 2095–2101.
[79] Lombardi, G., & Stronati, M. (2005). Infezione congenita da citomegalovirus [Congenital cytomegalovirus infection]. Minerva pediatrica, 57 (5), 213–227.
[80] O'Connor, S., Taylor, C., Campbell, L. A., Epstein, S., & Libby, P. (2001). Potential infectious etiologies of atherosclerosis: a multifactorial perspective. Emerging infectious diseases, 7 (5), 780–788.
[81] Dal Canto, A. J., & Virgin, H. W., 4th (2000). Animal models of infection-mediated vasculitis: implications for human disease. International journal of cardiology, 75 Suppl 1, S37–S52.
[82] Prasad, A., Zhu, J., Halcox, J. P., Waclawiw, M. A., Epstein, S. E., & Quyyumi, A. A. (2002). Predisposition to atherosclerosis by infections: role of endothelial dysfunction. Circulation, 106 (2), 184–190.
[83] Zhu, J., Nieto, F. J., Horne, B. D., Anderson, J. L., Muhlestein, J. B., & Epstein, S. E. (2001). Prospective study of pathogen burden and risk of myocardial infarction or death. Circulation, 103 (1), 45–51.
[84] Hsich, E., Zhou, Y. F., Paigen, B., Johnson, T. M., Burnett, M. S., & Epstein, S. E. (2001). Cytomegalovirus infection increases development of atherosclerosis in Apolipoprotein-E knockout mice. Atherosclerosis, 156 (1), 23–28.
[85] Cousins, S. W., Espinosa-Heidmann, D. G., Miller, D. M., Pereira-Simon, S., Hernandez, E. P., Chien, H., Meier-Jewett, C., & Dix, R. D. (2012). Macrophage activation associated with chronic murine cytomegalovirus infection results in more severe experimental choroidal neovascularization. PLoS pathogens, 8 (4), e1002671.
[86] Gerna, G., Percivalle, E., Baldanti, F., Sozzani, S., Lanzarini, P., Genini, E., Lilleri, D., & Revello, M. G. (2000). Human cytomegalovirus replicates abortively in polymorphonuclear leukocytes after transfer from infected endothelial cells via transient microfusion events. Journal of virology, 74 (12), 5629–5638.
[87] Knight, D. A., Waldman, W. J., & Sedmak, D. D. (1999). Cytomegalovirus-mediated modulation of adhesion molecule expression by human arterial and microvascular endothelial cells. Transplantation, 68 (11), 1814–1818.
[88] Cebulla, C. M., Miller, D. M., Knight, D. A., Briggs, B. R., McGaughy, V., & Sedmak, D. D. (2000). Cytomegalovirus induces sialyl Lewis (x) and Lewis (x) on human endothelial cells. Transplantation, 69 (6), 1202–1209.
[89] Panova I. E., Tonkih N. A., Prokop'eva M. Ju., Bukhtijarova N. V. (2004). Age-related macular degeneration with neovascular response: clinical features, characteristic of cell-mediated immunity. Vestnik Orenburgskogo gosudarstvennogo universiteta, 5: 124–6.
[90] Wyględowska-Promieńska, D., Piotrowska-Gwóźdź, A., Piotrowska-Seweryn, A., Mazur-Piotrowska, G., & Rokicki, W. (2014). Combination of bevacizumab and bromfenac therapy in age-related macular degeneration: a pilot study. Medical science monitor: international medical journal of experimental and clinical research, 20, 1168–1175.
[91] Sen, M., Honavar, S. G., Sharma, N., & Sachdev, M. S. (2021). COVID-19 and Eye: A Review of Ophthalmic Manifestations of COVID-19. Indian journal of ophthalmology, 69 (3), 488–509.
[92] Ramlall, V., Thangaraj, P. M., Meydan, C., Foox, J., Butler, D., Kim, J., May, B., De Freitas, J. K., Glicksberg, B. S., Mason, C. E., Tatonetti, N. P., & Shapira, S. D. (2020). Immune complement and coagulation dysfunction in adverse outcomes of SARS-CoV-2 infection. Nature medicine, 26 (10), 1609–1615.
[93] Bikdeli, B., Madhavan, M. V., Jimenez, D., Chuich, T., Dreyfus, I., Driggin, E., Nigoghossian, C., Ageno, W., Madjid, M., Guo, Y., Tang, L. V., Hu, Y., Giri, J., Cushman, M., Quéré, I., Dimakakos, E. P., Gibson, C. M., Lippi, G., Favaloro, E. J., Fareed, J.,… Global COVID-19 Thrombosis Collaborative Group, Endorsed by the ISTH, NATF, ESVM, and the IUA, Supported by the ESC Working Group on Pulmonary Circulation and Right Ventricular Function (2020). COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. Journal of the American College of Cardiology, 75 (23), 2950–2973.
[94] Becker R. C. (2020). COVID-19 update: COVID-19-associated coagulopathy. Journal of thrombosis and thrombolysis, 50 (1), 54–67.
[95] Varga, Z., Flammer, A. J., Steiger, P., Haberecker, M., Andermatt, R., Zinkernagel, A. S., Mehra, M. R., Schuepbach, R. A., Ruschitzka, F., & Moch, H. (2020). Endothelial cell infection and endotheliitis in COVID-19. Lancet (London, England), 395 (10234), 1417–1418.
[96] Raval, N., Djougarian, A., & Lin, J. (2021). Central retinal vein occlusion in the setting of COVID-19 infection. Journal of ophthalmic inflammation and infection, 11, 10.
[97] Walinjkar, J. A., Makhija, S. C., Sharma, H. R., Morekar, S. R., & Natarajan, S. (2020). Central retinal vein occlusion with COVID-19 infection as the presumptive etiology. Indian journal of ophthalmology, 68 (11), 2572–2574.
[98] Sheth, J. U., Narayanan, R., Goyal, J., & Goyal, V. (2020). Retinal vein occlusion in COVID-19: A novel entity. Indian journal of ophthalmology, 68 (10), 2291–2293.
[99] Invernizzi, A., Pellegrini, M., Messenio, D., Cereda, M., Olivieri, P., Brambilla, A. M., & Staurenghi, G. (2020). Impending Central Retinal Vein Occlusion in a Patient with Coronavirus Disease 2019 (COVID-19). Ocular immunology and inflammation, 28 (8), 1290–1292.
[100] Yahalomi, T., Pikkel, J., Arnon, R., & Pessach, Y. (2020). Central retinal vein occlusion in a young healthy COVID-19 patient: A case report. American journal of ophthalmology case reports, 20, 100992.
[101] Dumitrascu, O. M., Volod, O., Bose, S., Wang, Y., Biousse, V., & Lyden, P. D. (2020). Acute ophthalmic artery occlusion in a COVID-19 patient on apixaban. Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association, 29 (8), 104982.
[102] Tisdale, A. K., & Chwalisz, B. K. (2020). Neuro-ophthalmic manifestations of coronavirus disease 19. Current opinion in ophthalmology, 31 (6), 489–494.
[103] François, J., Collery, A. S., Hayek, G., Sot, M., Zaidi, M., Lhuillier, L., & Perone, J. M. (2021). Coronavirus Disease 2019-Associated Ocular Neuropathy With Panuveitis: A Case Report. JAMA ophthalmology, 139 (2), 247–249.
[104] Rodrigo-Armenteros, P., Uterga-Valiente, J. M., Zabala-Del-Arco, J., Taramundi-Argüeso, S., Antón-Méndez, L., Gómez-Muga, J. J., & Garcia-Monco, J. C. (2021). Optic neuropathy in a patient with COVID-19 infection. Acta neurologica Belgica, 1–3.
[105] Kedar, S., Jayagopal, L. N., & Berger, J. R. (2019). Neurological and Ophthalmological Manifestations of Varicella Zoster Virus. Journal of neuro-ophthalmology: the official journal of the North American Neuro-Ophthalmology Society, 39 (2), 220–231.
[106] Sawalha, K., Adeodokun, S., & Kamoga, G. R. (2020). COVID-19-Induced Acute Bilateral Optic Neuritis. Journal of investigative medicine high impact case reports, 8, 2324709620976018.
[107] Ignatiev S. A, Alekseev I. B, & Nam Ya. A. (2018). Military and Medical Expertise in Patients with Central Retinal Degeneration. International Journal Of Clinical And Experimental Medical Sciences, 4 (4), 68.
[108] V. K. Khavinson, S. V. Trofimova. (2000). Peptide bioregulators in ophthalmology. Saint Petersburg: Foliant.
[109] Stolyarenko G. Y., Tyurina M. I, Khalaym A. V. (2006). “Invasive therapy of the pathology of the macular area of the retina”, Macula: Thesis in collection of reports in the II All Russian seminar - "round table". Rostov-on-Don. pp. 379-380.
[110] Ignatyev S. A., Alekseev I. B., Chernakova G. M., Kleshcheva E. A., & Nam Yu. A. (2015). Age-related Macular Degeneration and the Cytomegalovirus: Controversial Issues of Pathogenesis. Russian Ophthalmological Journal, 4, 71-78.
Author Information
  • Consulting Department, City Clinical Hospital Named by S. P. Botkin, Department of Health, Moscow, Russian Federation

  • State Clinical Hospital Named by S. P. Botkin, Moscow City Ophthalmological Center, Moscow, Russian Federation; Federal State Budgetary Educational Institution of Further Professional Education Russian Medical Academy of Continuous Professional Education, Ministry of Healthcare of the Russian Federation, Moscow, Russia Federation

  • Federal State Budgetary Educational Institution of Further Professional Education Russian Medical Academy of Continuous Professional Education, Ministry of Healthcare of the Russian Federation, Moscow, Russia Federation; Main Military Clinical Hospital Named After N. N. Burdenko, Moscow, Russia Federation

  • Branch №2, Federal Budgetary Institution of Healthcare, Medical Rehabilitation Centre, Ministry of Economic Development of Russia, Moscow, Russian Federation

  • Federal State Budgetary Educational Institution of Further Professional Education Russian Medical Academy of Continuous Professional Education, Ministry of Healthcare of the Russian Federation, Moscow, Russia Federation

Cite This Article
  • APA Style

    Sergey Aleksandrovich Ignatiev, Igor’ Borisovich Alekseev, Sergey Petrovich Kazakov, Yuliya Arkadievna Nam, Aleksandr Ivanovich Listratov. (2021). Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19. International Journal of Clinical and Experimental Medical Sciences, 7(5), 127-137. https://doi.org/10.11648/j.ijcems.20210705.11

    Copy | Download

    ACS Style

    Sergey Aleksandrovich Ignatiev; Igor’ Borisovich Alekseev; Sergey Petrovich Kazakov; Yuliya Arkadievna Nam; Aleksandr Ivanovich Listratov. Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19. Int. J. Clin. Exp. Med. Sci. 2021, 7(5), 127-137. doi: 10.11648/j.ijcems.20210705.11

    Copy | Download

    AMA Style

    Sergey Aleksandrovich Ignatiev, Igor’ Borisovich Alekseev, Sergey Petrovich Kazakov, Yuliya Arkadievna Nam, Aleksandr Ivanovich Listratov. Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19. Int J Clin Exp Med Sci. 2021;7(5):127-137. doi: 10.11648/j.ijcems.20210705.11

    Copy | Download

  • @article{10.11648/j.ijcems.20210705.11,
      author = {Sergey Aleksandrovich Ignatiev and Igor’ Borisovich Alekseev and Sergey Petrovich Kazakov and Yuliya Arkadievna Nam and Aleksandr Ivanovich Listratov},
      title = {Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19},
      journal = {International Journal of Clinical and Experimental Medical Sciences},
      volume = {7},
      number = {5},
      pages = {127-137},
      doi = {10.11648/j.ijcems.20210705.11},
      url = {https://doi.org/10.11648/j.ijcems.20210705.11},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ijcems.20210705.11},
      abstract = {This article highlights main aspects of pathogenesis of age-related macular degeneration (AMD) and the connection between SARS-CoV-2 and diseases of the posterior pole of the eyes. Background: A novel coronavirus disease COVID-19 is actual nowadays due to its multiple organ damage, including eye tissues. Retina is also a target organ. AMD is the most common cause of central vision loss and its development is connected not only with ageing, but also with some other factors. Last years ophthalmological community considers virus infection to be a predictor and trigger for developing of AMD. Objective: Several theories have been proposed for the development of AMD. The most common theories are vascular due to pathogenetically significant decrease in blood flow in the pool of the carotid arteries; metabolic disorders (systemic and local); oxidative stress in endothelial cells; hereditary predisposition. Inflammation as a pathogenetic mechanism appeared in a novel light of discoveries in developing of not only AMD, but also some other eye diseases. The connection between SARS-CoV-2 and diseases of the posterior pole known nowadays are conjunctivitis, central retinal vein occlusion, isolated inflammatory optic neuritis, acute bilateral demyelinating optic neuritis. Thus, the question is still open. Conclusion: no single theory of the development of AMD can absolutely explain the diversity of pathological changes in of the retina and choroid tissues. Further study of the role of each factor of pathogenesis– from molecular to tissue will allow the development of fundamentally novel and perspective directions of AMD therapy.},
     year = {2021}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Some Features of the Development of AMD and Other Diseases of the Posterior Pole Associated with the Virus Carrier and the Novel Coronavirus Disease COVID-19
    AU  - Sergey Aleksandrovich Ignatiev
    AU  - Igor’ Borisovich Alekseev
    AU  - Sergey Petrovich Kazakov
    AU  - Yuliya Arkadievna Nam
    AU  - Aleksandr Ivanovich Listratov
    Y1  - 2021/09/27
    PY  - 2021
    N1  - https://doi.org/10.11648/j.ijcems.20210705.11
    DO  - 10.11648/j.ijcems.20210705.11
    T2  - International Journal of Clinical and Experimental Medical Sciences
    JF  - International Journal of Clinical and Experimental Medical Sciences
    JO  - International Journal of Clinical and Experimental Medical Sciences
    SP  - 127
    EP  - 137
    PB  - Science Publishing Group
    SN  - 2469-8032
    UR  - https://doi.org/10.11648/j.ijcems.20210705.11
    AB  - This article highlights main aspects of pathogenesis of age-related macular degeneration (AMD) and the connection between SARS-CoV-2 and diseases of the posterior pole of the eyes. Background: A novel coronavirus disease COVID-19 is actual nowadays due to its multiple organ damage, including eye tissues. Retina is also a target organ. AMD is the most common cause of central vision loss and its development is connected not only with ageing, but also with some other factors. Last years ophthalmological community considers virus infection to be a predictor and trigger for developing of AMD. Objective: Several theories have been proposed for the development of AMD. The most common theories are vascular due to pathogenetically significant decrease in blood flow in the pool of the carotid arteries; metabolic disorders (systemic and local); oxidative stress in endothelial cells; hereditary predisposition. Inflammation as a pathogenetic mechanism appeared in a novel light of discoveries in developing of not only AMD, but also some other eye diseases. The connection between SARS-CoV-2 and diseases of the posterior pole known nowadays are conjunctivitis, central retinal vein occlusion, isolated inflammatory optic neuritis, acute bilateral demyelinating optic neuritis. Thus, the question is still open. Conclusion: no single theory of the development of AMD can absolutely explain the diversity of pathological changes in of the retina and choroid tissues. Further study of the role of each factor of pathogenesis– from molecular to tissue will allow the development of fundamentally novel and perspective directions of AMD therapy.
    VL  - 7
    IS  - 5
    ER  - 

    Copy | Download

  • Sections