Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (778 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The three possible sequences of codons by which genetic translation may occur from one nucleotide sequence. A segment of mRNA 5'auccga3' could be translated as 5'AUC.. or 5'UCC.. or 5'CCG.., depending on the location of the start codon.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Frame, Reading; Frames, Reading; Reading Frame.
Where it fits in the MeSH classification
- Broader topics
- Genetic Code
- Narrower topics
- Open Reading Frames
- See also
- Codon
Related concepts
- Codon
- Protein Biosynthesis
- Auccga3
- Start Codon
Research landscape
PubMed indexes 31,703 records tagged with the MeSH heading “Reading Frames” (counts retrieved 2026-10-29). 3,067 of them (9.7%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 9,961 records.
Reviews account for 964 records (3.0%) and meta-analyses for 10. Randomized controlled trials number 5 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,282 |
| 2000-2009 | 9,961 |
| 2010-2019 | 9,393 |
| 2020 onward | 3,067 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 964 | 3.0% |
| Meta-analyses | 10 | 0.0% |
| Randomized controlled trials | 5 | 0.0% |
Method: PubMed query "Reading Frames"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Penaeid shrimp genome provides insights into benthic adaptation and frequent molting | 2019 | Research article Design not recorded in structured metadata | 329 | cc by PMID 30664654 · DOI · PMC6341167 |
| Discovery and Genomic Characterization of a 382-Nucleotide Deletion in ORF7b and ORF8 during the Early Evolution of SARS-CoV-2 | 2020 | Research article Design not recorded in structured metadata | 250 | cc by PMID 32694143 · DOI · PMC7374062 |
| SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death | 2018 | Research article Design not recorded in structured metadata | 198 | cc by PMID 30185776 · DOI · PMC6125346 |
| A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42392077 · DOI · PMC13429030 |
Penaeid shrimp genome provides insights into benthic adaptation and frequent molting [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Crustacea, the subphylum of Arthropoda which dominates the aquatic environment, is of major importance in ecology and fisheries.
- Closing excerpt
- vannamei genome not only provides an insight into the genetic underpinnings of specific biological processes, but also provides valuable information for enhancing crustacean aquaculture.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)
Crustacea, the subphylum of Arthropoda which dominates the aquatic environment, is of major importance in ecology and fisheries. Here we report the genome sequence of the Pacific white shrimp Litopenaeus vannamei, covering ~1.66 Gb (scaffold N50 605.56 Kb) with 25,596 protein-coding genes and a high proportion of simple sequence repeats (>23.93%). The expansion of genes related to vision and locomotion is probably central to its benthic adaptation. Frequent molting of the shrimp may be explained by an intensified ecdysone signal pathway through gene expansion and positive selection. As an important aquaculture organism, L. vannamei has been subjected to high selection pressure during the past 30 years of breeding, and this has had a considerable impact on its genome. Decoding the L. vannamei genome not only provides an insight into the genetic underpinnings of specific biological processes, but also provides valuable information for enhancing crustacean aquaculture.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30664654 · DOI · PMC6341167
Discovery and Genomic Characterization of a 382-Nucleotide Deletion in ORF7b and ORF8 during the Early Evolution of SARS-CoV-2 [2]
Abstract reading summary — source excerpts
- Opening excerpt
- To date, limited genetic changes in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genome have been described.
- Closing excerpt
- In addition to providing a key insight into the evolutionary behavior of SARS-CoV-2 as the virus adapts to its new human hosts, the emergence of ORF8 deletion variants may also impact vaccination strategies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (341 words)
To date, limited genetic changes in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genome have been described. Here, we report a 382-nucleotide (nt) deletion in SARS-CoV-2 that truncates open reading frame 7b (ORF7b) and ORF8, removing the ORF8 transcription regulatory sequence (TRS) and eliminating ORF8 transcription. The earliest 382-nt deletion variant was detected in Singapore on 29 January 2020, with the deletion viruses circulating in the country and accounting for 23.6% (45/191) of SARS-CoV-2 samples screened in this study. SARS-CoV-2 with the same deletion has since been detected in Taiwan, and other ORF7b/8 deletions of various lengths, ranging from 62 nt to 345 nt, have been observed in other geographic locations, including Australia, Bangladesh, and Spain. Mutations or deletions in ORF8 of SARS-CoV have been associated with reduced replicative fitness and virus attenuation. In contrast, the SARS-CoV-2 382-nt deletion viruses showed significantly higher replicative fitness in vitro than the wild type, while no difference was observed in patient viral load, indicating that the deletion variant viruses retained their replicative fitness. A robust antibody response to ORF8 has been observed in SARS-CoV-2 infection, suggesting that the emergence of ORF8 deletions may be due to immune-driven selection and that further deletion variants may emerge during the sustained transmission of SARS-CoV-2 in humans.IMPORTANCE During the SARS epidemic in 2003/2004, a number of deletions were observed in ORF8 of SARS-CoV, and eventually deletion variants became predominant, leading to the hypothesis that ORF8 was an evolutionary hot spot for adaptation of SARS-CoV to humans. However, due to the successful control of the SARS epidemic, the importance of these deletions for the epidemiological fitness of SARS-CoV in humans could not be established. The emergence of multiple SARS-CoV-2 strains with ORF8 deletions, combined with evidence of a robust immune response to ORF8, suggests that the lack of ORF8 may assist with host immune evasion. In addition to providing a key insight into the evolutionary behavior of SARS-CoV-2 as the virus adapts to its new human hosts, the emergence of ORF8 deletion variants may also impact vaccination strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32694143 · DOI · PMC7374062
SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The molecular mechanisms underlying the severe lung pathology that occurs during SARS-CoV infections remain incompletely understood.
- Closing excerpt
- In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (165 words)
The molecular mechanisms underlying the severe lung pathology that occurs during SARS-CoV infections remain incompletely understood. The largest of the SARS-CoV accessory protein open reading frames (SARS 3a) oligomerizes, dynamically inserting into late endosomal, lysosomal, and trans-Golgi-network membranes. While previously implicated in a non-inflammatory apoptotic cell death pathway, here we extend the range of SARS 3a pathophysiologic targets by examining its effects on necrotic cell death pathways. We show that SARS 3a interacts with Receptor Interacting Protein 3 (Rip3), which augments the oligomerization of SARS 3a helping drive necrotic cell death. In addition, by inserting into lysosomal membranes SARS 3a triggers lysosomal damage and dysfunction. Consequently, Transcription Factor EB (TFEB) translocates to the nucleus increasing the transcription of autophagy- and lysosome-related genes. Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly. In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30185776 · DOI · PMC6125346
A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Virological research has traditionally focused on individual viruses or viral families.
- Closing excerpt
- Together, the viral ORFeome provides a scalable framework for dissecting viral protein function across the breadth of the virome.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (127 words)
Virological research has traditionally focused on individual viruses or viral families. Advances in DNA synthesis now allow large-scale construction of individual gene products, enabling systematic exploration of the virome. Here, we developed a barcoded library of ∼12,000 viral open reading frames (vORFs) from 513 viral species, which we leveraged to identify hundreds of viral regulators of cellular proliferation, MHC class I antigen presentation, and interferon signaling. Integrating results across these screens revealed unique phenotypic profiles and functional vORF modules, allowing the in-depth characterization of two previously uncharacterized viral proteins, MC162R and Yaba-like disease virus (YLDV) 151R, which impair MHC class I antigen presentation and interferon (IFN)-β signaling, respectively. Together, the viral ORFeome provides a scalable framework for dissecting viral protein function across the breadth of the virome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42392077 · DOI · PMC13429030
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Upstream open reading frames as regulators of mRNA translation [5]
- Research article Reading m6A in the Transcriptome: m6A-Binding Proteins [6]
- Research article Entries in the Leiden Duchenne muscular dystrophy mutation database: an overview of mutation types and paradoxical cases that confirm the reading-frame rule [7]
- Research article Emerging evidence for functional peptides encoded by short open reading frames [8]
- Research article Transposable elements in cancer [9]
- Research article Gene expression regulation by upstream open reading frames and human disease [10]
References
- Zhang X, Yuan J, Sun Y, Li S, Gao Y, Yu Y, et al.. Penaeid shrimp genome provides insights into benthic adaptation and frequent molting. . 2019. PMID 30664654 · DOI · PMC6341167
- Su YCF, Anderson DE, Young BE, Linster M, Zhu F, Jayakumar J, et al.. Discovery and Genomic Characterization of a 382-Nucleotide Deletion in ORF7b and ORF8 during the Early Evolution of SARS-CoV-2. . 2020. PMID 32694143 · DOI · PMC7374062
- Yue Y, Nabar NR, Shi CS, Kamenyeva O, Xiao X, Hwang IY, et al.. SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death. . 2018. PMID 30185776 · DOI · PMC6125346
- Fujimura E, O'Leary CN, Li MZ, Roberts RA, Glassman CR, Paulo JA, et al.. A viral ORFeome library for systems-level genetic dissection of host-pathogen interactions. . 2026. PMID 42392077 · DOI · PMC13429030
- Morris DR, Geballe AP. Upstream open reading frames as regulators of mRNA translation. Mol Cell Biol. 2000. PMID 11073965 · DOI · PMC86464
- Patil DP, Pickering BF, Jaffrey SR. Reading m6A in the Transcriptome: m6A-Binding Proteins. Trends Cell Biol. 2018. PMID 29103884 · DOI · PMC5794650
- Aartsma-Rus A, Van Deutekom JC, Fokkema IF, Van Ommen GJ, Den Dunnen JT. Entries in the Leiden Duchenne muscular dystrophy mutation database: an overview of mutation types and paradoxical cases that confirm the reading-frame rule. Muscle Nerve. 2006. PMID 16770791 · DOI
- Andrews SJ, Rothnagel JA. Emerging evidence for functional peptides encoded by short open reading frames. Nat Rev Genet. 2014. PMID 24514441 · DOI
- Burns KH. Transposable elements in cancer. Nat Rev Cancer. 2017. PMID 28642606 · DOI
- Barbosa C, Peixeiro I, Romão L. Gene expression regulation by upstream open reading frames and human disease. PLoS Genet. 2013. PMID 23950723 · DOI · PMC3738444
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.