SARS-CoV-2 Mutation Detail Information

Virus Mutation SARS-CoV-2 Mutation delH69/V70


Basic Characteristics of Mutations
Mutation Site delH69/V70
Mutation Site Sentence We report severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike DeltaH69/V70 in multiple independent lineages; often occurring after acquisition of receptor binding motif replacements such as N439K and Y453F; known to increase binding affinity to the ACE2 receptor and confer antibody escape.
Mutation Level Amino acid level
Mutation Type Deletion
Gene/Protein/Region S
Standardized Encoding Gene S  
Genotype/Subtype B.1.1.7
Viral Reference MN908947.3
Functional Impact and Mechanisms
Disease COVID-19    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 34166617
Title Recurrent emergence of SARS-CoV-2 spike deletion H69/V70 and its role in the Alpha variant B.1.1.7
Author Meng B,Kemp SA,Papa G,Datir R,Ferreira IATM,Marelli S,Harvey WT,Lytras S,Mohamed A,Gallo G,Thakur N,Collier DA,Mlcochova P,Duncan LM,Carabelli AM,Kenyon JC,Lever AM,De Marco A,Saliba C,Culap K,Cameroni E,Matheson NJ,Piccoli L,Corti D,James LC,Robertson DL,Bailey D,Gupta RK
Journal Cell reports
Journal Info 2021 Jun 29;35(13):109292
Abstract We report severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike DeltaH69/V70 in multiple independent lineages, often occurring after acquisition of receptor binding motif replacements such as N439K and Y453F, known to increase binding affinity to the ACE2 receptor and confer antibody escape. In vitro, we show that, although DeltaH69/V70 itself is not an antibody evasion mechanism, it increases infectivity associated with enhanced incorporation of cleaved spike into virions. DeltaH69/V70 is able to partially rescue infectivity of spike proteins that have acquired N439K and Y453F escape mutations by increased spike incorporation. In addition, replacement of the H69 and V70 residues in the Alpha variant B.1.1.7 spike (where DeltaH69/V70 occurs naturally) impairs spike incorporation and entry efficiency of the B.1.1.7 spike pseudotyped virus. Alpha variant B.1.1.7 spike mediates faster kinetics of cell-cell fusion than wild-type Wuhan-1 D614G, dependent on DeltaH69/V70. Therefore, as DeltaH69/V70 compensates for immune escape mutations that impair infectivity, continued surveillance for deletions with functional effects is warranted.
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.