TY  - JOUR
AU  - Lundstrom, Kenneth
AU  - Hromić-Jahjefendić, Altijana
AU  - Bilajac, Esma
AU  - Aljabali, Alla
AU  - Baralić, Katarina
AU  - Sabri, Nagwa
AU  - Shehata, Eslam
AU  - Raslan, Mohamed
AU  - Ferreira, Ana Cláudia
AU  - Orlandi, Lidiane
AU  - Serrano-Aroca, Ángel
AU  - Tambuwala, Murtaza
AU  - Uversky, Vladimir
AU  - Azevedo, Vasco
AU  - Alzahrani, Khalid
AU  - Alsharif, Khalaf
AU  - Halawani, Ibrahim
AU  - Alzahrani, Fuad
AU  - Redwan, Elrashdy
AU  - Barh, Debmalya
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4317
AB  - The COVID-19 pandemic has been the focus of research the past two years. The major breakthrough was made by discovering pathways related to SARS-CoV-2 infection through cellular interaction by angiotensin-converting enzyme (ACE2) and cytokine storm. The presence of ACE2 in lungs, intestines, cardiovascular tissues, brain, kidneys, liver, and eyes shows that SARS-CoV-2 may have targeted these organs to further activate intracellular signalling pathways that lead to cytokine release syndrome. It has also been reported that SARS-CoV-2 can hijack coatomer protein-I (COPI) for S protein retrograde trafficking to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), which, in turn, acts as the assembly site for viral progeny. In infected cells, the newly synthesized S protein in endoplasmic reticulum (ER) is transported first to the Golgi body, and then from the Golgi body to the ERGIC compartment resulting in the formation of specific a motif at the C-terminal end. This review summarizes major events of SARS-CoV-2 infection route, immune response following host-cell infection as an important factor for disease outcome, as well as comorbidity issues of various tissues and organs arising due to COVID-19. Investigations on alterations of host-cell machinery and viral interactions with multiple intracellular signaling pathways could represent a major factor in more effective disease management.
PB  - Elsevier Inc.
T2  - Cellular Signalling
T1  - COVID-19 signalome: Pathways for SARS-CoV-2 infection and impact on COVID-19 associated comorbidity
VL  - 101
DO  - 10.1016/j.cellsig.2022.110495
ER  - 

@article{
author = "Lundstrom, Kenneth and Hromić-Jahjefendić, Altijana and Bilajac, Esma and Aljabali, Alla and Baralić, Katarina and Sabri, Nagwa and Shehata, Eslam and Raslan, Mohamed and Ferreira, Ana Cláudia and Orlandi, Lidiane and Serrano-Aroca, Ángel and Tambuwala, Murtaza and Uversky, Vladimir and Azevedo, Vasco and Alzahrani, Khalid and Alsharif, Khalaf and Halawani, Ibrahim and Alzahrani, Fuad and Redwan, Elrashdy and Barh, Debmalya",
year = "2023",
abstract = "The COVID-19 pandemic has been the focus of research the past two years. The major breakthrough was made by discovering pathways related to SARS-CoV-2 infection through cellular interaction by angiotensin-converting enzyme (ACE2) and cytokine storm. The presence of ACE2 in lungs, intestines, cardiovascular tissues, brain, kidneys, liver, and eyes shows that SARS-CoV-2 may have targeted these organs to further activate intracellular signalling pathways that lead to cytokine release syndrome. It has also been reported that SARS-CoV-2 can hijack coatomer protein-I (COPI) for S protein retrograde trafficking to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC), which, in turn, acts as the assembly site for viral progeny. In infected cells, the newly synthesized S protein in endoplasmic reticulum (ER) is transported first to the Golgi body, and then from the Golgi body to the ERGIC compartment resulting in the formation of specific a motif at the C-terminal end. This review summarizes major events of SARS-CoV-2 infection route, immune response following host-cell infection as an important factor for disease outcome, as well as comorbidity issues of various tissues and organs arising due to COVID-19. Investigations on alterations of host-cell machinery and viral interactions with multiple intracellular signaling pathways could represent a major factor in more effective disease management.",
publisher = "Elsevier Inc.",
journal = "Cellular Signalling",
title = "COVID-19 signalome: Pathways for SARS-CoV-2 infection and impact on COVID-19 associated comorbidity",
volume = "101",
doi = "10.1016/j.cellsig.2022.110495"
}

Lundstrom, K., Hromić-Jahjefendić, A., Bilajac, E., Aljabali, A., Baralić, K., Sabri, N., Shehata, E., Raslan, M., Ferreira, A. C., Orlandi, L., Serrano-Aroca, Á., Tambuwala, M., Uversky, V., Azevedo, V., Alzahrani, K., Alsharif, K., Halawani, I., Alzahrani, F., Redwan, E.,& Barh, D.. (2023). COVID-19 signalome: Pathways for SARS-CoV-2 infection and impact on COVID-19 associated comorbidity. in Cellular Signalling
Elsevier Inc.., 101.
https://doi.org/10.1016/j.cellsig.2022.110495

Lundstrom K, Hromić-Jahjefendić A, Bilajac E, Aljabali A, Baralić K, Sabri N, Shehata E, Raslan M, Ferreira AC, Orlandi L, Serrano-Aroca Á, Tambuwala M, Uversky V, Azevedo V, Alzahrani K, Alsharif K, Halawani I, Alzahrani F, Redwan E, Barh D. COVID-19 signalome: Pathways for SARS-CoV-2 infection and impact on COVID-19 associated comorbidity. in Cellular Signalling. 2023;101.
doi:10.1016/j.cellsig.2022.110495 .

Lundstrom, Kenneth, Hromić-Jahjefendić, Altijana, Bilajac, Esma, Aljabali, Alla, Baralić, Katarina, Sabri, Nagwa, Shehata, Eslam, Raslan, Mohamed, Ferreira, Ana Cláudia, Orlandi, Lidiane, Serrano-Aroca, Ángel, Tambuwala, Murtaza, Uversky, Vladimir, Azevedo, Vasco, Alzahrani, Khalid, Alsharif, Khalaf, Halawani, Ibrahim, Alzahrani, Fuad, Redwan, Elrashdy, Barh, Debmalya, "COVID-19 signalome: Pathways for SARS-CoV-2 infection and impact on COVID-19 associated comorbidity" in Cellular Signalling, 101 (2023),
https://doi.org/10.1016/j.cellsig.2022.110495 . .