Overview

rs74956615 is a genetic variant on gene RAVER1 associated with Covid-19.

This variant is located on chromosome 19. The variations at position 10317045 are the genetic letters A/A, A/T

Since humans have each twice (one from each parent), these letter-variations occur on both chromosomes. People can have the same or different letters on both chromosomes. Every person's individual variation combination is referred to as genotype. For variant rs74956615 there are 2 currently known genotypes : A/A or A/T

Short Overview

Variant Location

rs74956615 is located on gene RAVER1 in chromsome 19. Use the genome browser to explore the location of rs74956615 and its genetic neighbourhood.

Conditions & Traits

rs74956615 affects the following conditions and traits:

Pathogenicity

rs74956615 affects the following conditions:

Pharmacogenetics

We do not have any data that links rs74956615 to any drugs.

Diagnostics

rs74956615 is commonly tested together with other variants on the same gene.

Genome Browser

This interactive browser visualizes what no human can see with the naked eye - our DNA. From a down to a specific position on a . The position you are looking at here is the exact location of variant rs on gene RAVER1. Explore more variants and their effects on the body by browsing left and right along the DNA strand.

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Did you know genetic variants affect drugs?

Mutations are changes in genes and genetic variations are differences in the DNA among people. Variants are tiny changes in just one piece of the DNA while haplotypes are groups of these changes that usually come together.

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Dr. Wallerstorfer

Conditions & Traits of rs74956615

The different genotypes of variant rs74956615 can affect the likelyhood of developing certain traits or conditions. Current research shows that 1 condition and 0 traits are associated with rs74956615. The following table shows the relationship between genotypes and conditions and traits.

Did you know genetic variants affect drugs?

Genetic variants can influence how our body reacts to certain drugs. The presence of specific genetic variants can increase or decrease the efficiency and effectiveness of a drug, impacting how well it works inside our system. Additionally, certain genetic variants can heighten or lessen the toxicity of a drug, thereby affecting the risk of unwanted side effects. They can also alter how a drug is metabolized, which influences the appropriate dosage one should receive.

doctor_quote

Dr. Wallerstorfer

Variant Table Legend

Clinical Testing

Scientific Studies

Biological Male Symbol

Biological Female Symbol

Unisex Symbol for both Genders

Classification of Variants

Variants can be classified either based on clinical tests or scientific studies. In the classification based on clinical tests, the variants are divided into five categories from Disease Causing (harmful) to No Effect (not harmful). This classification is based on family histories, laboratory tests and computer predictions and is intended to help doctors make medical decisions. The aim is to recognize the immediate health impact of variants on the human body. Classification based on scientific studies, however, is about understanding the long-term effects. It aims to identify the influence of genetic variants in conditions, traits, and evolution. Variants are classified into different categories based on their functional impact: Loss-of-Function (reduced gene activity), Gain-of-Function (increased gene activity), Neutral (no significant impact) and Evolutionary Conservation. This classification uses experimental data, population studies, and computational analyses.

Genotype

A

A

Level of evidence

Increased likelihood

Unisex

2 Sources

Participants: 2094879

The genotype with the letters A/A is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.

Genotype

A

T

Level of evidence

Increased likelihood

Unisex

2 Sources

Participants: 2094879

The genotype with the letters A/T is considered a risk factor for developing the disease. Carriers of this genetic result are at increased risk of developing the disease.

Diagnostics

rs74956615 is commonly tested together with other variants on the same gene.

Related variants

Diseases and traits are often influenced by multiple genetic variants. To better understand how genetics affects certain diseases and traits, it is important to consider these additional factors. The following table shows other variants that are also associated with the same diseases and traits as rs74956615.

Genotype Distribution

Knowing your genome can actually tell you a lot about your ancestors.

The prevalence of the different genotypes is based on the native inhabitants of a region. In the map below you see how common each genotype is in the native inhabitants of those regions. Since genetic material is passed down form generation to generation, your DNA shows traces of the geographical origins of your ancestors.

This data is based on “The 1000 Genomes Project” which established one of the most detailed overviews of human genetic variations across the globe. The regions are broadly categorized into five continental groups: Africa, America, Europe, South Asia and East Asia. All continental groups together display the global prevalence. Click through the regions, to learn more about the local prevalence of the possible genotypes.

At present, there is no distribution data available for SNP 74956615. 74956615.

The Genotype Distribution in the selected area is:
Legend:
Included regions
Excluded regions
no-data

Studies and Sources

All of the resources below examine variant rs74956615

The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease. (11/17/16)

William J Astle, Heather Elding, Tao Jiang, Dave Allen, Dace Ruklisa, Alice L Mann, Daniel Mead, Heleen Bouman, Fernando Riveros-Mckay, Myrto A Kostadima, John J Lambourne, Suthesh Sivapalaratnam, Kate Downes, Kousik Kundu, Lorenzo Bomba, Kim Berentsen, John R Bradley, Louise C Daugherty, Olivier Delaneau, Kathleen Freson, Stephen F Garner, Luigi Grassi, Jose Guerrero, Matthias Haimel, Eva M Janssen-Megens, Anita Kaan, Mihir Kamat, Bowon Kim, Amit Mandoli, Jonathan Marchini, Joost H A Martens, Stuart Meacham, Karyn Megy, Jared O'Connell, Romina Petersen, Nilofar Sharifi, Simon M Sheard, James R Staley, Salih Tuna, Martijn van der Ent, Klaudia Walter, Shuang-Yin Wang, Eleanor Wheeler, Steven P Wilder, Valentina Iotchkova, Carmel Moore, Jennifer Sambrook, Hendrik G Stunnenberg, Emanuele Di Angelantonio, Stephen Kaptoge, Taco W Kuijpers, Enrique Carrillo-de-Santa-Pau, David Juan, Daniel Rico, Alfonso Valencia, Lu Chen, Bing Ge, Louella Vasquez, Tony Kwan, Diego Garrido-Martín, Stephen Watt, Ying Yang, Roderic Guigo, Stephan Beck, Dirk S Paul, Tomi Pastinen, David Bujold, Guillaume Bourque, Mattia Frontini, John Danesh, David J Roberts, Willem H Ouwehand, Adam S Butterworth, Nicole Soranzo

PubMed: 27863252
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