Viruses are obligate intracellular parasites with limited genome and thereby rely on the host cell machinery for their proliferation. Thereby viruses have evolved molecular strategies to escape the cellular innate immune surveillance and to usurp/hijack the host cell signaling to create a microenvironment conducive for viral dissemination.  Most often the virus-mediated alterations to the host signaling or the response to infection paves way for the pathogenesis of the viral disease. Understanding these interactions will help in identifying the molecular mechanisms that drive viral diseases

The cellular mitochondria, membranes and cytoskeleton are primary targets of many viruses. Mitochondria serve as the hub for many cellular events and mitochondrial dynamics is considered an integral cellular process with implications in cellular homeostasis, metabolism, inflammation and innate immunity. Thus many viruses target/exploit the host mitochondria to escape cellular defense mechanisms and promote viral proliferation. The physiological perturbation associated with viral infection also affect the host mitochondria.

The complex interplay between the virus and the cellular mitochondria and the subsequent consequence on mitochondrial- metabolism,  antiviral and inflammatory signaling governs the outcome of viral infection and viral disease pathogenesis.  The complex interplay between the viruses and the host machinery or organelle such as mitochondria is an ever expanding and unexplored area. Characterizing these interactions will unravel the molecular cues that promote viral dissemination and disease pathogenesis.

Currently the lab is working with the flaviviruses, Dengue virus (DENV), Hepatitis C virus (HCV) and Japanese Encephalitis virus (JEV). During the pandemic  we  have also worked towards COVID-19 research and isolated local circulating strains of SARS-CoV2 and are conducting studies for repurposing of approved drugs against SARS-CoV2. We are also in the pursuit of screening compounds effective against DENV and JEV.  In future we will also attempt to characterize the virus-host interactions in the pursuit of identifying therapeutic targets with pan-viral potential.

The major focus areas of the lab are;

1. Characterize the virus-host interaction (with focus on interactions between viruses and cellular mitochondria, peroxisome, cytoskeleton and intracellular trafficking components).
2. Elucidate the virus-host interactions that predispose to disease pathogenesis.
3. Characterize the molecular events in HCV, DENV and JEV life cycle such as the entry, replication, assembly and secretion of virus particle to identify pro-viral host factors.
4. Identify potential therapeutic targets and develop effective strategies to curb viral dissemination and disease pathogenesis.
5. Screen for potential anti-viral compounds and elucidate their mode of action.

2022

1. Agarwal A, Alam MF, Basu B, Pattanayak S, Asthana S, Syed GH*, Kalia M*, Vrati S*. Japanese Encephalitis Virus NS4A Protein Interacts with PTEN-Induced Kinase 1 (PINK1) and Promotes Mitophagy in Infected Cells. Microbiol Spectr. 2022 May 23:e0083022. doi: 10.1128/spectrum.00830-22
2. Taraphdar D, Singh B, Pattanayak S, Kiran A, Kokavalla P, Alam MF and Syed GH. Comodulation of Dengue and Chikungunya Virus Infection During a Coinfection Scenario in Human Cell Lines. Front. Cell. Infect. Microbiol. 2022. 12:821061. doi: 10.3389/fcimb.2022.821061
3. Singh B, Avula K, Chatterjee S, Datey A, Ghosh A, De S, …..Syed GH* & Chattopadhyay S*. Isolation and Characterization of SARS-CoV-2 strains circulating in Eastern India. Front. Cell. Infect. Microbiol. 2022 (in press)

2021

1. Panda S, Behera S, Alam MF, Syed GH. Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses. Mitochondrion. 2021; 227-242.
2. Kumar S, Singh B, Kumari P, Kumar PV, Agnihotri G, Khan S, Beuria TK, Syed GH*, Dixit A*. Identification of multipotent drugs for COVID-19 therapeutics with the evaluation of their SARS-CoV2 inhibitory activity. Computational and Structural Biotechnology Journal. 2021, 19, 1998-2017.
3. Suresh V, Mohanty V, Avula K, …….Syed GH*, Senapati S*. Quantitative proteomics of hamster lung tissues infected with SARS-CoV-2 reveal host factors having implication in the disease pathogenesis and severity. FASEB J. 2021 Jul;35(7):e21713. doi: 10.1096/fj.202100431R.
4. Avula K, Singh B, Vijay Kumar P, Syed GH. Role of Lipid Transfer Proteins (LTPs) in the Viral Life Cycle. Frontiers in Microbiology. 2021, 12, 1493.

2020

1. Raghav S, Ghosh A, Turuk J, …….. Syed GH, Dixit A, Prasad P; Odisha COVID-19 Study Group; ILS COVID-19 Team, Pati S, Parida A. Analysis of Indian SARS-CoV-2 Genomes Reveals Prevalence of D614G Mutation in Spike Protein Predicting an Increase in Interaction With TMPRSS2 and Virus Infectivity. Front Microbiol. 2020 Nov 23;11:594928. doi: 10.3389/fmicb.2020.594928.

2018

1. Kim S-J, Ahn D-G, Syed GH, Siddiqui A. The essential role of mitochondrial dynamics in antiviral immunity. Mitochondrion. 2018, 41, 21-27.

2017

1. Syed GH (co-corresponding author), Khan M, Yang S, Siddiqui A. Hepatitis C virus lipoviroparticles (HCV-LVP) assemble in the endoplasmic reticulum (ER) and bud off from the ER to Golgi in COPII vesicles. J Virol. 2017, doi: 10.1128/JVI.00499-17.
2. Börgeson E, Wallenius V, Syed GH, Darshi M, Lantero Rodriguez J, Biörserud C, Ragnmark Ek M, Björklund P, Quiding-Järbrink M, Fändriks L, Godson C, Sharma K. AICAR ameliorates high-fat diet-associated pathophysiology in mouse and ex vivo models, independent of adiponectin. Diabetologia. 2017, 60(4):729-739. doi: 10.1007/s00125-017-4211-9

2016

1. Khan M, Syed GH, Kim SJ, Siddiqui A. Hepatitis B Virus-Induced Parkin-Dependent Recruitment of Linear Ubiquitin Assembly Complex (LUBAC) to Mitochondria and Attenuation of Innate Immunity. PLoS Pathog. 2016, 12(6):e1005693. doi: 10.1371/journal.ppat.1005693

2015

1. Till A, Saito R, Merkurjev D, Liu JJ, Syed GH, Kolnik M, Siddiqui A, Glas M, Scheffler B, Ideker T, Subramani S. 2015. Evolutionary trends and functional anatomy of the human expanded autophagy network. Autophagy 11(9):1652-67.
2. Borgeson E, Johnsson A, Lee YS, Till A, Syed GH, Ali-Shah ST, Guiry PJ, Dalli J, Colas RA, Serhan NC, Sharma K, Godson C. Lipoxin A4 attenuates obesity-induced adipose inflammation and associated liver and kidney disease. 2015. Cell Metabolism 22(1):125-37.
3. Khan M, Syed GH, Seong-Jun K and Siddiqui A. 2015. Mitochondrial Dynamics and Viral infections: a close nexus. 2015. Biochim Biophys Acta Molecular Cell Research 1853 (10 Pt B): 2822-33.

2014

1. Soto-Acosta R, Bautista-Carbajal P, Syed GH, Siddiqui A, Del Angel MR. 2014. Nordihydroguaiaretic acid (NDGA) inhibits replication and viral morphogenesis of Dengue virus. Antiviral Research, 109:132-40
2. Seong-Jun K, Syed GH (equal contribution), Khan M, Chiu W, Sohail AM, Gish GR, & Siddiqui A. 2014. Hepatitis C Virus Triggers Mitochondrial Fission and Attenuates Apoptosis to Promote Viral Persistence. Proc. Natl. Acad. Sci, 111:6413-8.
3. Syed GH, Tang H (equal contribution), Khan M, Hassanein T, Liu J, & Siddiqui A. 2014. Hepatitis C Virus stimulates Density Lipoprotein Receptor (LDLR) expression to facilitate viral propagation. J. Virol, 88:2519-29.

2013

1. Seong-Jun K, Syed GH, Siddiqui A. 2013. Hepatitis C virus induces mitochondrial translocation of Parkin and subsequent mitophagy. PLoS Pathog, 9(3):e1003285.
2. Yadaiah M, Sudhamalla B, Rao PN, Roy KR, Ramakrishna D, Syed GH, Ramaiah KV, AK bhuyan. 2013. Arrested Cell Proliferation through Cysteine Protease Activity of Eukaryotic Ribosomal Protein S4. FASEB J, 27:803-10.

2012

1. Bishé B, Syed GH, Field SJ, Siddiqui A. 2012. Role of phosphatidylinositol 4-phosphate (PI4P) and its binding protein GOLPH3 in hepatitis C virus secretion. J Biol Chem, 287, 27637-47.
2. Bishe B, Syed GH, Siddiqui A. 2012. Phosphoinositides in the Hepatitis C virus Life Cycle. Viruses, 4, 2340-58.

2011

1. Syed GH, Siddiqui A. 2011. Effects of hypolipidemic agent nordihydroguaiaretic acid on lipid droplets and hepatitis C virus. Hepatology, 54, 1936-46.
2. Amako Y, Syed GH (equal contribution), Siddiqui A. 2011. Protein kinase D negatively regulates hepatitis C virus secretion through phosphorylation of oxysterol binding protein and ceramide transfer protein. J Biol Chem, 286, 11265-274.

2010

1. Syed GH, Amako Y, Siddiqui A. 2010. Hepatitis C virus hijacks host lipid metabolism. Trends Endocrinol Metab, 21: 33-40.

2007

1. Syed GH, Ramaiah KVA. 2007. Reduced eIF2alpha phosphorylation and increased proapoptotic proteins in aging. Biochem Biophys Res Commun, 355:365-70.
2. Syed GH, Ramaiah KVA. 2007. Endoplasmic reticulum: Stress, signaling and apoptosis. Current Science, 93: 1684-96.

Book Chapters

1. Syed GH, Wyles DL and Siddiqui A. 2014. Chapter on ‘Hepatitis Viruses’ in the Reference Module in Biomedical Sciences. Elsevier. doi: 10.1016/B978-0-12-801238-3.00087-8.
2. Seong-Jun K, Syed GH, Sohail M, Khan M and Siddiqui A. Chapter on ‘The Emerging Role of Mitochondrial Dynamics in Viral Hepatitis’ in the book ‘Mitochondria in Liver Disease’ by Neil Kaplowitz and Derick Han published by CRC press.

• In 2014 was awarded the Ramalingswami Re-entry Fellowship from the Dept. of Biotechnology, Govt of India (Fellowship not availed).
• In June-2015 was awarded the Wellcome Trust-DBT India Alliance Intermediate Fellowship.

Students who are interested in pursuing research & training in the field of virus-host interactions and molecular virology are welcome to pursue suitable programs in the Virus-Host Interaction Lab

• Prospective PhD students should look for the PhD Program advertisement on the ILS Website. Students having their own research fellowship are preferred.
• Candidates who wish to apply postdoctoral fellowships (IA, N-PDF, DBT RA, ICMR) in the lab focus areas may contact Dr. G Syed (gulamsyed@ils.res.in).
• Students who wants to pursue summer training (3 months) and Master’s project (1yr to 6 months) can contact Dr. G Syed (gulamsyed@ils.res.in).