Ifi44, an interferon-alfa inducible protein, is associated with the immune response, especially in relation to viral and bacterial infections [1,2]. It may be involved in interferon-related pathways, as it is encoded by an interferon-stimulated gene. Its biological importance lies in its potential roles in immune regulation and response to pathogens, making it a gene of interest in immunological research [1,2,3].

In in vitro studies, Ifi44 inhibits HIV-1 replication by suppressing HIV-1 LTR promoter activity, affecting viral transcription. Depletion of endogenous Ifi44 in J-LAT cells induces reactivation of latent HIV-1, suggesting that Ifi44 may play a role in maintaining HIV-1 latency [1]. In patients with rheumatoid arthritis (RA), Ifi44 is identified as a hub gene and an immune evasion biomarker for SARS-CoV-2 and Staphylococcus aureus infection. It negatively regulates the IFN signaling pathway to promote viral replication and bacterial proliferation [2]. In head and neck squamous cell carcinoma (HNSCC), ACSL4 upregulates Ifi44 expression, promoting cell proliferation and invasiveness [3]. Also, in systemic lupus erythematosus (SLE) and lupus nephritis (LN), Ifi44 is identified as a biomarker with its expression levels correlated with disease-related indicators [4,5,6,7,8].

In conclusion, Ifi44 is significantly involved in immune-related biological functions, especially in response to viral and bacterial infections, as well as in cancer development. Its role in maintaining HIV-1 latency, promoting immune evasion in RA patients, and its association with SLE and LN, as revealed through various in vitro and human-based studies, highlights its importance in understanding these disease mechanisms.