Genetic Basis for Mucormycosis Progression in COVID-19 Patients: From Susceptibility to Severity

被引:0
作者
Muruganantham, Jethendra Kumar [1 ]
Veerabathiran, Ramakrishnan [1 ]
机构
[1] Chettinad Acad Res & Educ, Chettinad Hosp & Res Inst, Fac Allied Hlth Sci, Human Cytogenet & Genom Lab, Kelambakkam 603103, Tamilnadu, India
来源
INFECTIOUS DISEASES & IMMUNITY | 2024年 / 4卷 / 02期
关键词
COVID-19; Mucormycosis; Pathogenesis; Genetics basis; VIRAL ENTRY; MECHANISMS;
D O I
10.1097/ID9.0000000000000115
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
The dynamics of COVID-19 and mucormycosis reveal a complex interplay of genetic factors that influence the susceptibility, severity, and immune responses. COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits an increased incidence of mucormycosis, particularly in individuals with comorbidities or corticosteroid therapy. Mucormycosis is a fungal infection that affects the sinuses, orbits, and lungs and demands timely intervention with antifungal medications and surgery because of its life-threatening nature. Research on the genetic underpinnings of this intersection has unveiled key insights into the pathogenicity of Mucorales. Breakthroughs in genetic tools have exposed virulence factors, such as the CotH protein family and high-affinity iron-uptake mechanisms. Genetic susceptibility is a pivotal element in identifying individuals at risk of developing COVID-19, facilitating early detection, and allowing for personalized treatment strategies. DPP9, MIF, and TYK2 are among the genes implicated in COVID-19 severity, emphasizing the intricate relationship between genetic makeup and viral response. The genetic landscape extends to viral entry mechanisms, thereby affecting infection efficiency. Specific polymorphisms in genes such as IFNAR2, OAS3, and TYK2 are associated with COVID-19 severity, indicating shared genetic bases between severe and hospitalized cases. Mucormycosis is genetically predisposed, particularly in immunocompromised individuals. The challenge lies in understanding the genetic factors influencing susceptibility and offering insights into pathogenesis and potential therapeutic avenues. Organ transplantation adds another layer, increasing susceptibility to infections such as COVID-19 and mucormycosis. The impact of immunosuppression on COVID-19 severity remains elusive, necessitating ongoing research on the immunological mechanisms. Despite the challenges posed by emerging SARS-CoV-2 variants, the intricate connection between genetic factors and the interplay of COVID-19 and mucormycosis presents an opportunity for personalized treatment, targeted interventions, and refined public health strategies.
引用
收藏
页码:86 / 92
页数:7
相关论文
共 45 条
[1]   Targeting the GRP78-Dependant SARS-CoV-2 Cell Entry by Peptides and Small Molecules [J].
Allam, Loubna ;
Ghrifi, Fatima ;
Mohammed, Hakmi ;
El Hafidi, Naima ;
El Jaoudi, Rachid ;
El Harti, Jaouad ;
Lmimouni, Badreddine ;
Belyamani, Lahcen ;
Ibrahimi, Azeddine .
BIOINFORMATICS AND BIOLOGY INSIGHTS, 2020, 14
[2]   Mucormycosis in 2023: an update on pathogenesis and management [J].
Alqarihi, Abdullah ;
Kontoyiannis, Dimitrios P. ;
Ibrahim, Ashraf S. .
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY, 2023, 13
[3]   Editorial: Host Genetics in Viral Pathogenesis and Control [J].
An, Ping ;
Guo, Ju-Tao ;
Winkler, Cheryl A. .
FRONTIERS IN GENETICS, 2019, 10
[4]   Risk factors for Coronavirus disease-associated mucormycosis [J].
Arora, Umang ;
Priyadarshi, Megha ;
Katiyar, Varidh ;
Soneja, Manish ;
Garg, Prerna ;
Gupta, Ishan ;
Bharadiya, Vishwesh ;
Berry, Parul ;
Ghosh, Tamoghna ;
Patel, Lajjaben ;
Sarda, Radhika ;
Garg, Shreya ;
Agarwal, Shubham ;
Arora, Veronica ;
Ramprasad, Aishwarya ;
Kumar, Amit ;
Garg, Rohit Kumar ;
Kodan, Parul ;
Nischal, Neeraj ;
Singh, Gagandeep ;
Jorwal, Pankaj ;
Kumar, Arvind ;
Baitha, Upendra ;
Meena, Ved Prakash ;
Ray, Animesh ;
Sethi, Prayas ;
Xess, Immaculata ;
Vikram, Naval ;
Sinha, Sanjeev ;
Biswas, Ashutosh ;
Thakar, Alok ;
Bhatnagar, Sushma ;
Trikha, Anjan ;
Wig, Naveet .
JOURNAL OF INFECTION, 2022, 84 (03) :383-390
[5]   Genetic clues to COVID susceptibility and severity [J].
Asgari, Samira ;
Pousaz, Lionel A. .
NATURE, 2021, 600 (7889) :390-391
[6]   COVID-19 and comorbidities: A role for dipeptidyl peptidase 4 (DPP4) in disease severity? [J].
Bassendine, Margaret F. ;
Bridge, Simon H. ;
McCaughan, Geoffrey W. ;
Gorrell, Mark D. .
JOURNAL OF DIABETES, 2020, 12 (09) :649-658
[7]   Genetic susceptibility to severe COVID-19 [J].
Cappadona, Claudio ;
Rimoldi, Valeria ;
Paraboschi, Elvezia Maria ;
Asselta, Rosanna .
INFECTION GENETICS AND EVOLUTION, 2023, 110
[8]   An integrated genomic and transcriptomic survey of mucormycosis-causing fungi [J].
Chibucos, Marcus C. ;
Soliman, Sameh ;
Gebremariam, Teclegiorgis ;
Lee, Hongkyu ;
Daugherty, Sean ;
Orvis, Joshua ;
Shetty, Amol C. ;
Crabtree, Jonathan ;
Hazen, Tracy H. ;
Etienne, Kizee A. ;
Kumari, Priti ;
O'Connor, Timothy D. ;
Rasko, David A. ;
Filler, Scott G. ;
Fraser, Claire M. ;
Lockhart, Shawn R. ;
Skory, Christopher D. ;
Ibrahim, Ashraf S. ;
Bruno, Vincent M. .
Nature Communications, 2016, 7
[9]   SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues [J].
D'Antonio, Matteo ;
Nguyen, Jennifer P. ;
Arthur, Timothy D. ;
Matsui, Hiroko ;
D'Antonio-Chronowska, Agnieszka ;
Frazer, Kelly A. .
CELL REPORTS, 2021, 37 (07)
[10]   Virus entry: Molecular mechanisms and biomedical applications [J].
Dimitrov, DS .
NATURE REVIEWS MICROBIOLOGY, 2004, 2 (02) :109-122