Biology subjects

Mohan, M.

Publications and source records attributed to Mohan, M..

13 recordsLinked to original sources

bioRxiv2026

Leveraging collaborations between researchers, wildlife managers and citizen-volunteers to monitor endangered carnivore populations across space and time

Monitoring populations is fundamental for conserving threatened carnivores, but can be difficult to sustain in the long term across large landscapes. We present a collaborative framework for monitoring dholes (Cuon alpinus) in India's Western Ghats, combining fecal DNA-based individual identification, Spatially Explicit Capture-Recapture (SECR) models, state Forest Department participation, and trained citizen-volunteers. We surveyed across six sites between 2019-2023, encompassing three Protected Areas (Wayanad, Parambikulam, Periyar) and their adjacent Territorial Divisions. Fecal samples were genotyped using a panel of 96 Single Nucleotide Polymorphisms, and detections were analyzed using SECR models to estimate densities. In Wayanad Sanctuary, densities remained stable across 2019, 2022 and 2023, increasing marginally from 15.67 to 19.01 individuals per 100 sq.km. In 2023, densities varied substantially among six sites, from 9.73/100 sq.km in Parambikulam to 29.23 in Nemmara Territorial Division. Field implementation involved an average of 46 Forest Department personnel co-collecting data per site-year. Among former citizen-volunteers who were surveyed for project feedback (N=29), 83% went on to either work or pursue higher education in wildlife-related or -adjacent fields. We demonstrate that molecular individual identification coupled with SECR can provide a practical basis for dhole population assessments while enabling multi-stakeholder participation in field monitoring. Sustained engagement with wildlife managers and locally recruited volunteers can strengthen institutional capacity, facilitate knowledge exchange, and improve continuity of monitoring programs. We argue that integrating molecular ecology with collaborative governance and democratizing field-science offers a scalable pathway for landscape-level monitoring required to guide dhole conservation.

ecology↗

bioRxiv2026

APOBEC3G Splicing Defects in Nonhuman Primate Models Result in Disparate Viral Mutational Profiles Relative to Humans

Nonhuman primates (NHPs), particularly macaques, are indispensable models for studying human infectious diseases due to their close immunological and physiological similarities. Understanding species-specific molecular differences is essential for maximizing the translational value of these models. Here we report that APOBEC3G (A3G), a potent antiviral restriction factor and the major source of genetic variations in HIV, exhibits a widespread mRNA splicing defect in the Cercopithecinae subfamily, which includes the commonly used NHP models. Driven by intronic polymorphisms, this splicing defect substantially reduces A3G protein levels and consequently results in a markedly reduced A3G-mediated mutation signatures, fewer defective viral genomes, and greater viral diversification in SIV compared to HIV. This species-specific effect is not restricted to lentiviruses: reduced A3G signatures have also been reported in simian foamy virus and simian T-cell leukemia virus, suggesting broader effects across primate retroviruses. These findings reveal a lineage-specific alteration in a major antiviral restriction factor, with important implications for viral restriction, evolution, drug resistance, and immune evasion. They also highlight the importance of incorporating naturally occurring genetic variation into NHP model selection to improve the reproducibility, translational fidelity, and biological relevance of preclinical research.

genomics↗

bioRxiv2026

An approach for single-amino-acid resolution epitope mapping by kinetic affinity screening of antibody drugs against biosensor on-chip library of deep mutationally-scanned target variants

Epitope mapping is central to rational antibody drug design, affinity optimization and the anticipation of therapeutic resistance mechanisms. Here, we demonstrate the use of Sensor Integrated Proteome on Chip (SPOC) technology for single amino acid resolution epitope mapping. By generating high throughput (HTP) binding kinetics data, we identify important residues within the target epitope whose mutations alter drug-target interactions. The SPOC platform integrates simultaneous HTP cell-free production of folded proteins in nanowells from immobilized plasmid DNAs or linear expression cassettes and capture onto biosensor chips for subsequent label-free binding kinetic analysis using surface plasmon resonance (SPR). The model system comprised the extracellular domain (ECD) of CD20, a membrane-spanning 4-domain family protein, screened against its FDA-approved therapeutic monoclonal antibodies (thAbs) - rituximab and ocrelizumab. Using our proprietary POC protein nanofactory system, a partial deep mutationally scanned (DMS) CD20 ECD mutant library of 79 variants was produced on SPOC biosensor chips via rational single amino acid substitutions of the epitope and surrounding residues with alanine, aspartic acid, lysine, and serine, collectively representing four broad classes of amino acid side chain chemistries: nonpolar, acidic, basic, and polar neutral. The SPOC protein biosensor chip was then screened with both thAbs using SPOC SPR to generate kinetic affinity data, evaluate mutations that led to affinity loss or gain, and ultimately identify critical epitope residues that interface with the antibodies. Most mutations within the rituximab and ocrelizumab epitopes - EPANPSEK and YNCEPANPSEKNSPST, respectively - resulted in complete loss of binding or >25% increase in apparent KD. Notably, N171, P172, and S173 mutations, irrespective of side chain substitution, resulted in complete loss of rituximab binding while at least three diverse side chain substitutions at E168, P169, N171, P172, S173, E174, K175, and T180, led to complete loss of binding for ocrelizumab. These outcomes identify the listed residues as the most critical contact points for their respective antibodies. Interestingly, we also found that functional side-chain substitutions at some residues flanking the epitope increased affinity. This indicates that these non-epitope residues contribute to antibody contact, and that polarity at these sites is a tractable lever for affinity modulation by targeting the corresponding contact residues on the antibody CDRs. The proposed SPOC approach of screening drug candidates against on-chip library of mutationally-scanned therapeutic targets is relevant in the early phase of drug development to resolve epitopes at the residue-level to support more informed down-selection of candidates. It facilitates cost-effective improvement of thAbs, enhancing therapeutic efficacy across a wide array of therapeutic targets, including rare variants that might otherwise lead to therapeutic resistance.

immunology↗

bioRxiv2025

An approach to produce thousands of single-chain antibody variants on a SPR biosensor chip for measuring target binding kinetics and for deep characterization of antibody paratopes

Drug discovery continues to face a staggering 90% failure rate, with many setbacks occurring during late-stage clinical trials. To address this challenge, there is an increasing focus on developing and evaluating new technologies to enhance the "design" and "test" phases of antibody-based drugs (e.g., monoclonal antibodies, bispecifics, CAR-T therapies, ADCs) and biologics during early preclinical development, with the goal of identifying lead molecules with a higher likelihood of clinical success. Artificial intelligence (AI) is becoming an indispensable tool in this domain, both for improving molecules identified through traditional approaches and for the de novo design of novel therapeutics. However, critical bottlenecks persist in the "build" and "test" phases of AI-designed antibodies and protein binders, impeding early preclinical evaluation. While AI models can rapidly generate thousands to millions of putative drug designs, technological and cost limitations mean that only a few dozen candidates are typically produced and tested. Drug developers often face a tradeoff between ultra-high-throughput wet lab methods that provide binary yes/no binding data and biophysical methods that offer detailed characterization of a limited number of drug-target pairs. To address these bottlenecks, we previously reported the development of the Sensor-integrated Proteome On Chip (SPOC(R)) platform, which enables the production and capture-purification of 1,000 - 2,400 folded proteins directly onto a surface plasmon resonance (SPR) biosensor chip for measuring kinetic binding rates with picomolar affinity resolution. In this study, we extend the SPOC technology to the expression of single-chain antibodies (sc-antibodies), specifically scFv and VHH, and dual-chain Fab constructs. We demonstrate that these proteins are capture-purified at high levels on SPR biosensors and retain functionality as shown by the binding specificity to their respective target antigens, with affinities comparable to those reported in the literature. SPOC outputs comprehensive kinetic data including quantitative binding (Rmax), on-rate (ka), off-rate (kd), affinity (KD), and half-life (t1/2), for each of thousands of on-chip sc-antibodies. Additionally, we present a case study showcasing single amino acid mutational scan of the complementarity-determining regions (CDRs) of a HER2 VHH (nanobody) paratope. Using 92 unique mutated variants from four different amino acid substitutions, we pinpoint critical residues within the paratope that could further enhance binding affinity. This study serves as a demonstration of a novel high-throughput approach for biophysical screening of hundreds to thousands of single chain antibody sequences in a single assay, generating high affinity resolution kinetic data to support antibody discovery and AI-enabled pipelines.

immunology↗

bioRxiv2025

Rigorous process for isolation of gut-derived extracellular vesicles and the effect on latent HIV

AimExtracellular particles (EPs) are produced/secreted by cells from all domains of life and are present in all body fluids, brain, and gut. EPs consist of extracellular vesicles (EVs) made up of exosomes, microvesicles, and other membranous vesicles; and extracellular condensates (ECs) that are non-membranous carriers of lipid-protein-nucleic acid aggregates. The purity of EVs|ECs, which ultimately depends on the isolation method used to obtain them is critical, particularly EVs|ECs from the gastrointestinal (GI) tract that is colonized by a huge number of enteric bacteria. Therefore, identifying GI derived EVs|ECs of bacterial and host origin may serve as a window into the pathogenesis of diseases and as a potential therapeutic target. MethodsHere, we describe the use of high-resolution particle purification liquid chromatography (PPLC) gradient-bead-column integrated with polyvinylpolypyrrolidone (PVPP)-mediated extraction of impurities to isolate GI-derived EPs. Results and ConclusionPVPP facilitates isolation of pure and functionally active, non-toxic EVs ColEVs from colonic contents. ColEVs are internalized by cells and they activate HIV LTR promoter. In the absence of PVPP, ColEVs have a direct reductive potential of MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) absorbance in a cell-free system. Assessment of the origin of ColEVs reveals that they are composed of both bacteria and host particles. This protocol requires [~]12 hours (5 hours preprocessing, 7 hours isolation) to complete and should be used to purify EVs from sources contaminated with microbial agents to improve rigor. Additionally, this protocol provides a robust tool for researchers and clinicians investigating GI-derived EVs and the translational use of GI-derived EVs for diagnostic and therapeutic use. HighlightO_LIColEVs but not ColECs are present in colonic content (GI tract) and can be isolated with gradient or single bead PPLC column. C_LIO_LIColEVs isolated without PVPP are toxic to cells and they have a direct reductive potential of MTT. Addition of PVPP treatment in the isolation protocol results in clean and non-toxic ColEVs that transactivate the HIV LTR promoter. C_LI

molecular biology↗

bioRxiv2024

Epigenetic modulation of NLRP6 inflammasome sensor as a therapeutic modality to reduce necroptosis-driven gastrointestinal mucosal dysfunction in HIV/SIV infection

The epigenetic mechanisms driving persistent gastrointestinal mucosal dysfunction in HIV/SIV infection is an understudied topic. Using reduced-representation bisulfite sequencing, we identified HIV/SIV infection in combination anti-retroviral therapy (cART)-naive rhesus macaques (RMs) to induce marked hypomethylation throughout promoter-associated CpG islands (paCGIs) in genes related to inflammatory response (NLRP6, cGAS), cellular adhesion and proliferation in colonic epithelial cells (CEs). Moreover, low-dose delta-9-tetrahydrocannabinol (THC) administration reduced NLRP6 protein expression in CE by hypermethylating the NLRP6 paCGI and blocked polyI:C induced NLRP6 upregulation in vitro. In cART suppressed SIV-infected RMs, NLRP6 protein upregulation associated with significantly increased expression of necroptosis-driving proteins; phosphorylated-RIPK3(Ser199), phosphorylated-MLKL(Thr357/Ser358), and HMGB1. Most strikingly, supplementing cART with THC effectively reduced NLRP6 and necroptosis-driving protein expression to pre-infection levels. These findings for the first time demonstrate that NLRP6 upregulation and ensuing activation of necroptosis promote HIV/SIV-induced gastrointestinal mucosal dysfunction and that epigenetic modulation using phytocannabinoids represents a feasible therapeutic modality for alleviating HIV/SIV-induced gastrointestinal inflammation and associated comorbidities.

pathology↗

bioRxiv2024

Cannabinoids shift the basal ganglia miRNA m6A methylation profile towards an anti-inflammatory phenotype in SIV-infected Rhesus macaques

BackgroundEpitranscriptomic modifications modulate diverse biological processes like regulation of gene expression, abundance, location and function. N6-methyladenosine (m6A) methylation has been shown to regulate various diseases, including cancer and inflammation. While there is evidence that m6A modification is functionally relevant in neural development and differentiation, the role of m6A modification in HIV neuropathogenesis is unknown. MethodsHere, we used anti-N6-methyladenosine (m6A) antibody immunoprecipitation and microarray profiling to identify m6A modifications in miRNAs in basal ganglia (BG) of Rhesus macaques (RMs) that were uninfected (VEH) and SIV-infected on combination anti-retroviral therapy (cART) and either VEH-treated (VEH/SIV/cART), or THC:CBD-treated (THC:CBD/SIV/cART). Ingenuity pathway analysis was conducted to understand the biological implications of miRNA m6A methylation in HIV neuropathogenesis. Finally, to understand the functional significance of m6A modifications in miRNAs, we overexpressed FAM-labeled wild-type or m6A-modified miR-194-5p in SCC-25 cells and determined its impact on the expression of its target, STAT1, an interferon-stimulated transcription factor known to drive persistent neuroinflammation in several neurodegenerative diseases. ResultsHIV/SIV infection promoted an overall hypomethylated miRNA m6A profile. While the overall hypomethylated m6A profile was not significantly impacted by THC:CBD, specific miRNAs predicted to target proinflammatory genes showed markedly reduced m6A methylation levels compared to the VEH-treated RMs. Additionally, specific BG tissue miRNAs bearing m6A epi-transcriptomic marks were transferred and detected in BG-derived extracellular vesicles. Mechanistically, the DRACH motif in the seed region of miR-194-5p was significantly m6A hypomethylated in THC:CBD/SIV/cART RMs. In SCC-25 cells, unlike wild-type miR-194-5p, transfected m6A-modified miR-194-5p mimics failed to downregulate STAT1 protein expression. Further, compared to VEH/SIV/cART RMs, THC:CBD administration significantly reduced m6A methylation of 44 miRNAs directly involved in regulating CNS network genes. ConclusionsThese results underscore the need for investigating the qualitative, and posttranscriptional modifications in RNA along with the more traditional, quantitative alterations in pathological conditions or in response to disease modifying treatments. Our findings indicate that m6A epitranscriptomic marks in the seed nucleotide region can impair miRNA function and that cannabinoids may preserve it by reducing m6A methylation levels. Finally, these findings provide a novel mechanistic (miRNA m6A hypomethylation) explanation underlying the anti-neuroinflammatory effects of phytocannabinoids in HIV/SIV infection.

neuroscience↗

bioRxiv2024

Extracellular condensates (ECs) are endogenous modulators of HIV transcription and latency reactivation

Persistence of human immunodeficiency virus (HIV) latent reservoir is the major challenge to HIV cure because the latent reservoir is not eliminated by antiretroviral therapy (ART), and they serve as sources for viral rebound upon cessation of ART. Mechanisms regulating viral persistence are not well understood. This study used model systems of post-integration latency to explore the role of basal ganglia (BG) isolated extracellular condensates (ECs) in reprogramming HIV latent cells. We found that BG ECs from uninfected macaques (VEH) and SIV infected macaques (VEH|SIV) activate latent HIV transcription in various model systems. VEH and VEH|SIV ECs significantly increased expression of viral antigen in latently infected cells. Activation of viral transcription, antigen expression, and latency reactivation was inhibited by ECs from the brain of macaques treated with Delta-9-tetrahydrocannabinol (THC) and infected with SIV (THC|SIV). Virus produced by latently infected cells treated with VEH|SIV ECs potentiated cell-cell and cell-free HIV transmission. VEH|SIV ECs also reversed dexamethasone-mediated inhibition of HIV transcription while TNF-mediated reactivation of latency was reversed by THC|SIV ECs. Transcriptome and secretome analyses of total RNA and supernatants from latently infected cells treated with ECs revealed significant alteration in gene expression and cytokine secretion. THC|SIV ECs increased secretion of Th2 and decreased secretion of proinflammatory cytokines. Most strikingly, while VEH/SIV ECs robustly induced HIV RNA in latently HIV-infected cells, long-term low-dose THC administration enriched ECs for anti-inflammatory cargo that significantly diminished their ability to reactivate latent HIV, an indication that ECs are endogenous host factors that may regulate HIV persistence. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/613037v1_ufig1.gif" ALT="Figure 1"> View larger version (50K): org.highwire.dtl.DTLVardef@1d5e9fborg.highwire.dtl.DTLVardef@f48088org.highwire.dtl.DTLVardef@22696aorg.highwire.dtl.DTLVardef@136c0ae_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIECs isolated from SIV infected macaques (VEH|SIV ECs) is a positive regulator of LTR-dependent HIV transcription and production of infectious viral particles in vitro. C_LIO_LIECs isolated from THC treated SIV infected macaques (THC|SIV ECs) prevents the transcription and reactivation of HIV in latently infected cells and prevents production of viral particles in vitro. C_LIO_LIECs reprogram host transcriptome and secretome in manners that or suppress promote reactivation of latent HIV reservoir. C_LI The above highlights led to the conclusion that while VEH/SIV ECs robustly induced HIV RNA in latently HIV-infected cells, long-term low-dose THC administration enriched ECs for anti-inflammatory cargo that significantly diminished their ability to reactivate latent HIV.

cell biology↗

bioRxiv2024

Novel sensor-integrated proteome on chip (SPOC) platform with thousands of folded proteins on a 1.5 sq-cm biosensor chip to enable high-throughput real-time label-free screening for kinetic analysis.

An automated proteomic platform for producing and screening an array of functional proteins on biosensor surfaces was developed to address the challenges of measuring proteomic interaction kinetics in high throughput (HTP). This technology is termed Sensor-Integrated Proteome On Chip (SPOC(R)) which involves in-situ cell-free protein expression in nano-liter volume wells (nanowells) directly from rapidly customizable arrays of plasmid DNA, facilitating simultaneous capture-purification of up to 2400 unique full-length folded proteins onto a 1.5 sq-cm surface of a single gold biosensor chip. Arrayed SPOC sensors can then be screened by real-time label-free analysis, including surface plasmon resonance (SPR) to generate kinetic affinity, avidity data. Fluorescent and SPR assays were used to demonstrate zero crosstalk between protein spots. The functionality of the SPOC protein array was validated by antibody binding assay, post-translational modification, mutation-mediated differential binding kinetics, and catalytic activity screening on model SPOC protein arrays containing p53, Src, Jun, Fos, HIST1H3A, and SARS-CoV-2 receptor binding domain (RBD) protein variants of interest, among others. Monoclonal antibodies were found to selectively bind their target proteins on the SPOC array. A commercial anti-RBD antibody was used to demonstrate discriminatory binding to numerous SARS-CoV-2 RBD variants of concern with comprehensive kinetic information. With advantages of HTP, flexibility, low-cost, quick turnaround time, and real-time kinetic affinity profiling, the SPOC proteomic platform addresses the challenges of interrogating protein interactions at scale and can be deployed in various research and clinical applications.

systems biology↗

bioRxiv2023

DYRK1A interacts with Tuberous Sclerosis complex and promotes mTORC1 activity

DYRK1A, a ubiquitously expressed kinase, is linked to the dominant intellectual developmental disorder, microcephaly and Down syndrome in humans. It regulates numerous cellular processes such as cell cycle, vesicle trafficking and microtubule assembly. DYRK1A is a critical regulator of organ growth; however, how it regulates organ growth is not fully understood. Here, we show that the knockdown of DYRK1A results in reduced cell size, which depends on mTORC1. Using proteomic approaches, we found that DYRK1A interacts with the Tuberous sclerosis complex (TSC) proteins, namely TSC1 and TSC2, which negatively regulate mTORC1 activation. Further, we show that DYRK1A phosphorylates TSC2 at T1462, a modification known to inhibit TSC activity and promote mTORC1 activity. We also found that the reduced cell growth upon knockdown of DYRK1A can be rescued by overexpression of RHEB, an activator of mTORC1. Our findings suggest that DYRK1A inhibits TSC complex activity through inhibitory phosphorylation on TSC2, thereby promoting mTORC1 activity. Further, using the Drosophila neuromuscular junction as a model, we show that the mnb, the fly homologues of DYRK1A, is rescued by RHEB overexpression, suggesting a conserved role of DYRK1A in TORC1 regulation.

molecular biology↗

bioRxiv2021

Elucidation of the molecular interactions that enable stable interaction between HIV protease inhibitor ritonavir and human DNA repair enzyme ALKBH2: a molecular dynamics simulation study

The human DNA repair enzyme AlkB homologue-2 and 3 (ALKBH2 and ALKKBH3) repairs methyl adducts from genomic DNA. Overexpression of ALKBH2 and ALKBH3 has been implicated in both tumorigenesis and chemotherapy resistance in some cancers, including glioblastoma and renal cancer rendering it a potential therapeutic target and a diagnostic marker. However, no inhibitor is available against these important DNA repair proteins. Intending to repurpose a drug as an inhibitor of ALKBH2/ALKBH3, we performed in silico evaluation of HIV protease inhibitors and identified Ritonavir as an ALKBH2-interacting molecule. Using molecular dynamics simulation, we elucidated the molecular details of Ritonavir-ALKBH2 interaction. The present work highlights that Ritonavir might be used to target the ALKBH2-mediated DNA alkylation repair.

bioinformatics↗

bioRxiv2020

Insulin inhibits protein phosphatase 2A to impair β-adrenergic receptor function

Insulin impairs {beta}2-adrenergic receptor ({beta}2AR) function through G protein-coupled receptor kinase 2 (GRK2) by phosphorylation but less is known about dephosphorylation mechanisms mediated by protein phosphatase 2A (PP2A). Pharmacologic or genetic inhibition of phosphoinositide 3-kinase {gamma} (PI3K{gamma}) unexpectedly resulted in significant reduction of insulin-mediated {beta}2AR phosphorylation. Interestingly, {beta}2AR-associated phosphatase activity was inhibited by insulin but was reversed by knock-down of PI3K{gamma} showing negative regulation of PP2A by PI3K{gamma}. Co-immunoprecipitation and surface plasmon resonance studies using purified proteins showed that GRK2 and PI3K{gamma} form a complex and could be recruited to {beta}2ARs as GRK2 interacts with insulin receptor substrate following insulin treatment. Consistently, {beta}-blocker pretreatment did not reduce insulin-mediated {beta}2AR phosphorylation indicating agonist- and G{beta}{gamma}-independent non-canonical regulation of receptor function. Mechanistically, PI3K{gamma} inhibits PP2A activity at the {beta}AR complex by phosphorylating an intracellular inhibitor of PP2A (I2PP2A). Knock-down or CRISPR ablation of endogenous I2PP2A unlocked PP2A inhibition mediating {beta}2AR dephosphorylation showing an unappreciated acute regulation of PP2A in mediating insulin-{beta}2AR cross-talk. SummaryInsulin impairs {beta}2-adrenergic receptor ({beta}2AR) function through G protein-coupled receptor kinase 2 (GRK2). We show that insulin simultaneously inhibits protein phosphatase 2A (PP2A) sustaining {beta}2AR functional impairment. Unexpectedly, releasing PP2A inhibition by PI3K{gamma} preserves {beta}2AR function despite intact insulin-driven GRK2-mechanisms.

biochemistry↗

bioRxiv2020

Initial insights into the genetic epidemiology of SARS-CoV-2 isolates from Kerala suggest local spread from limited introductions

Coronavirus disease 2019 (COVID-19) rapidly spread from a city in China to almost every country in the world, affecting millions of individuals. Genomic approaches have been extensively used to understand the evolution and epidemiology of SARS-CoV-2 across the world. Kerala is a unique state in India well connected with the rest of the world through a large number of expatriates, trade, and tourism. The first case of COVID-19 in India was reported in Kerala in January 2020, during the initial days of the pandemic. The rapid increase in the COVID-19 cases in the state of Kerala has necessitated the understanding of the genetic epidemiology of circulating virus, evolution, and mutations in SARS-CoV-2. We sequenced a total of 200 samples from patients at a tertiary hospital in Kerala using COVIDSeq protocol at a mean coverage of 7,755X. The analysis identified 166 unique high-quality variants encompassing 4 novel variants and 89 new variants identified for the first time in SARS-CoV-2 samples isolated from India. Phylogenetic and haplotype analysis revealed that the circulating population of the virus was dominated (94.6% of genomes) by three distinct introductions followed by local spread, apart from identifying polytomies suggesting recent outbreaks. The genomes formed a monophyletic distribution exclusively mapping to the A2a clade. Further analysis of the functional variants revealed two variants in the S gene of the virus reportedly associated with increased infectivity and 5 variants that mapped to five primer/probe binding sites that could potentially compromise the efficacy of RT-PCR detection. To the best of our knowledge, this is the first and most comprehensive report of genetic epidemiology and evolution of SARS-CoV-2 isolates from Kerala.

genomics↗