SARS-CoV-2 Assembly: Gaining Infectivity and Beyond
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was responsible for causing the COVID-19 pandemic. Intensive research has illuminated the complex biology of SARS-CoV-2 and its continuous evolution during and after the COVID-19 pandemic. While much attention has been paid to the structur...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-10-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/16/11/1648 |
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| author | Harshita Katiyar Ariana Arduini Yichen Li Chen Liang |
| author_facet | Harshita Katiyar Ariana Arduini Yichen Li Chen Liang |
| author_sort | Harshita Katiyar |
| collection | DOAJ |
| description | Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was responsible for causing the COVID-19 pandemic. Intensive research has illuminated the complex biology of SARS-CoV-2 and its continuous evolution during and after the COVID-19 pandemic. While much attention has been paid to the structure and functions of the viral spike protein and the entry step of viral infection, partly because these are targets for neutralizing antibodies and COVID-19 vaccines, the later stages of SARS-CoV-2 replication, including the assembly and egress of viral progenies, remain poorly characterized. This includes insight into how the activities of the viral structural proteins are orchestrated spatially and temporally, which cellular proteins are assimilated by the virus to assist viral assembly, and how SARS-CoV-2 counters and evades the cellular mechanisms antagonizing virus assembly. In addition to becoming infectious, SARS-CoV-2 progenies also need to survive the hostile innate and adaptive immune mechanisms, such as recognition by neutralizing antibodies. This review offers an updated summary of the roles of SARS-CoV-2 structural proteins in viral assembly, the regulation of assembly by viral and cellular factors, and the cellular mechanisms that restrict this process. Knowledge of these key events often reveals the vulnerabilities of SARS-CoV-2 and aids in the development of effective antiviral therapeutics. |
| format | Article |
| id | doaj-art-a8a15f19838c431e93f7d2640156513a |
| institution | Kabale University |
| issn | 1999-4915 |
| language | English |
| publishDate | 2024-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj-art-a8a15f19838c431e93f7d2640156513a2024-11-26T18:25:06ZengMDPI AGViruses1999-49152024-10-011611164810.3390/v16111648SARS-CoV-2 Assembly: Gaining Infectivity and BeyondHarshita Katiyar0Ariana Arduini1Yichen Li2Chen Liang3Lady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, CanadaLady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, CanadaLady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, CanadaLady Davis Institute, Jewish General Hospital, Montreal, QC H3T 1E2, CanadaSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was responsible for causing the COVID-19 pandemic. Intensive research has illuminated the complex biology of SARS-CoV-2 and its continuous evolution during and after the COVID-19 pandemic. While much attention has been paid to the structure and functions of the viral spike protein and the entry step of viral infection, partly because these are targets for neutralizing antibodies and COVID-19 vaccines, the later stages of SARS-CoV-2 replication, including the assembly and egress of viral progenies, remain poorly characterized. This includes insight into how the activities of the viral structural proteins are orchestrated spatially and temporally, which cellular proteins are assimilated by the virus to assist viral assembly, and how SARS-CoV-2 counters and evades the cellular mechanisms antagonizing virus assembly. In addition to becoming infectious, SARS-CoV-2 progenies also need to survive the hostile innate and adaptive immune mechanisms, such as recognition by neutralizing antibodies. This review offers an updated summary of the roles of SARS-CoV-2 structural proteins in viral assembly, the regulation of assembly by viral and cellular factors, and the cellular mechanisms that restrict this process. Knowledge of these key events often reveals the vulnerabilities of SARS-CoV-2 and aids in the development of effective antiviral therapeutics.https://www.mdpi.com/1999-4915/16/11/1648SARS-CoV-2viral assemblystructural proteinsvirus–host interactions |
| spellingShingle | Harshita Katiyar Ariana Arduini Yichen Li Chen Liang SARS-CoV-2 Assembly: Gaining Infectivity and Beyond Viruses SARS-CoV-2 viral assembly structural proteins virus–host interactions |
| title | SARS-CoV-2 Assembly: Gaining Infectivity and Beyond |
| title_full | SARS-CoV-2 Assembly: Gaining Infectivity and Beyond |
| title_fullStr | SARS-CoV-2 Assembly: Gaining Infectivity and Beyond |
| title_full_unstemmed | SARS-CoV-2 Assembly: Gaining Infectivity and Beyond |
| title_short | SARS-CoV-2 Assembly: Gaining Infectivity and Beyond |
| title_sort | sars cov 2 assembly gaining infectivity and beyond |
| topic | SARS-CoV-2 viral assembly structural proteins virus–host interactions |
| url | https://www.mdpi.com/1999-4915/16/11/1648 |
| work_keys_str_mv | AT harshitakatiyar sarscov2assemblygaininginfectivityandbeyond AT arianaarduini sarscov2assemblygaininginfectivityandbeyond AT yichenli sarscov2assemblygaininginfectivityandbeyond AT chenliang sarscov2assemblygaininginfectivityandbeyond |