ReviewJournal of human immunity2026
Toward a monogenic architecture of human infections: From 1996 to 2026.
Review in Journal of human immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Autoantibodies neutralizing type I interferons underlie a third of cases of Chikungunya virus encephalitis or myelitis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Humans homozygous for rare or common hypomorphic IL23R variants are prone to tuberculosis.The Journal of experimental medicine · 2026Article
- Fungal Infections in Disorders of Inborn Errors of Immunity.Clinical reviews in allergy & immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
The provocative idea that a process as apparently complex as a lethal infection can be due to a cause as simple as a rare or common germline single-gene lesion has been documented over the last 30 years for a growing number of infections, and such variants have been diagnosed in an even larger number of patients. A monogenic lesion can predispose a healthy person, who has fended off other microbes, to death following infection with a specific microbe that has proved harmless in most other infected individuals. Remarkably, studies of monogenic infections led to the discovery that autoimmunity targeting the same component of host defense, sometimes due to another type of single-gene mutation, can also underlie the same infection. Both types of single-gene lesions are highly pleiotropic, depending on microbial challenges, and incompletely penetrant, depending on age. I discuss here the roots and implications of a monogenic architecture of life-threatening human infectious diseases, in terms of both basic biology and public health.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.