SARS-CoV-2 Mutation Detail Information

Virus Mutation SARS-CoV-2 Mutation D614G


Basic Characteristics of Mutations
Mutation Site D614G
Mutation Site Sentence D614G genotype of SARS-CoV-2 virus is highly infectious and responsible for almost all infection for 2nd wave.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region
Standardized Encoding Gene
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease COVID-19    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 34039497
Title An mRNA-based vaccine candidate against SARS-CoV-2 elicits stable immuno-response with single dose
Author Nag K,Chandra Baray J,Rahman Khan M,Mahmud A,Islam J,Myti S,Ali R,Haq Sarker E,Kumar S,Hossain Chowdhury M,Roy R,Islam F,Barman U,Khan H,Chakraborty S,Badsha A,Hossain M,Ahammad S,Rahman Chowdhury M,Ghosh P,Islam Shimul R,Ahmmed R,Hussain Bhuiya E,Kumar Biswas B,Mohiuddin M,Sultana N
Journal Vaccine
Journal Info 2021 Jun 23;39(28):3745-3755
Abstract D614G genotype of SARS-CoV-2 virus is highly infectious and responsible for almost all infection for 2nd wave. However, there are currently no reports with D614G as vaccine candidate. Here we report the development of an mRNA-LNP vaccine with D614G variant and characterization in animal model. We have used special mRNA-architecture and formulation that provides suitable response of the product. The surface plasmon resonance (SPR) data with spike protein (S) revealed that immunization generated specific antibody pools against the whole extracellular domain (RBD and S2) of the spike protein. The anti-sera and purified IgGs from immunized mice neutralized SARS-CoV-2-pseudoviruses in ACE2-expressing HEK293 cells in a dose dependent manner. Importantly, single-dose immunization protected mice-lungs from homotypic-pseudovirus entry and cytopathy. The immunologic responses have been implicated by a balanced and stable population of CD4+ cells with a Th1 bias. The data suggested great promise for immediate translation of the technology to the clinic.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.