It seems feasible that infectious diseases have a genetic background. Most propably is a genetic defect in an immune response gene. But they have been obviously overlooked in the last 50 years. A review Severe infectious diseases of childhood as monogenic inborn errors of immunity by Jean-Laurent Casanova in PNAS demonstrates that it has not penetrated the medicinal community that inborn errors leading to infectious disease are more than normal.
| Infectious Agent | disease | protein affected | Mutation |
| Plasmodium vivax | Duffy antigen and receptor for chemokine (DARC) | prevented disease | |
| HIV | CCR5 | prevented disease | |
| Norovirus | fucosyl transferase 2 (FUT2) | prevented disease | |
| Mycobacterium tuberculosis | Mycobacterial disease (MSMD) | IFN-γ and related proteins or receptors, IL12RB1 | caused disease |
| Neisseria | Menigitis | Complement C5-C9, factor D, properdin | caused disease |
| Human Papillovirus 5 (HPV-5) | Epidermodysplasia verruciformis | transmembrane channel-like 6 and 8 (TMC6 and TMC8) |
causing disease |
| Epstein-Barr virus | X-linked recessive lymphoproliferative disease (XLP) |
signaling lymphocytic activation molecule-associating protein (SAP) | causing disease |
| Candida albicans | chronic mucocutaneous candidiasis (CMC) | IL17F, IL-17 receptor A (IL17RA), IL17RC, actin-related gene 1 (ACT1) | causing disease |
| dermatophytes, Candida, Phialophora, Exophialia, and others |
Dermatophytosis (athlete’s foo) | caspase recruitment domain family member 9 (CARD9) |
causing disease |
| invasive pneumococcal disease (IPD) | NF-κB essential modulator (NEMO), IL-1R–associated kinase-4 (IRAK-4),myeloid differentiation primary response gene 88 (MyD88) | ||
| Herpex simplex | herpes simplex encephalits (HSE) | UNC93B1 and thus TLR-3 | causing disease |
| Trypanosoma evansi | apolipoprotein L-I (APOL1) | causing disase | |
| Influenza virus | influenza | IFN regulatory factor 7 (IRF7) | causing disease |
The review is very suggestive. I would like to point out, that infections where no inborn error has yet been found, should not be considered to have no genomic background. The list is too impressive already to be dismissed.
Since the paper is OPEN ACCESS a must!