# Gene Expression Profiles of Inflammatory Mediators in Influenza A and B Virus Infections: Insights from Riyadh, Saudi Arabia (2020–2023)

**Authors:** Noorah A. Alkubaisi, Mohamed A. Farrag, Ibrahim M. Aziz, Reem M. Aljowaie, Fahad N. Almajhdi

PMC · DOI: 10.3390/genes17030325 · Genes · 2026-03-17

## TL;DR

This study analyzed gene expression patterns of inflammatory mediators in influenza A and B infections in Saudi Arabia, revealing differences in immune responses and demographics.

## Contribution

The study provides subtype-specific cytokine profiles for influenza in Saudi Arabia, highlighting regional immune response differences.

## Key findings

- Influenza A/H3N2 showed increased prevalence from 2020 to 2023.
- Influenza A triggered higher IFN-α, IL-10, IL-13, and CCL-2 expression compared to B.
- Age and gender disparities were observed in infection rates and cytokine responses.

## Abstract

Background/Objectives: Influenza A (IAV) and influenza B (IBV) viruses pose significant public health threats, with varying epidemiology and immune responses. Limited subtype-specific cytokine data exist for influenza in Saudi Arabia. This study conducted molecular surveillance on 380 NPAs from patients at King Khalid University Hospital (KKUH) in Riyadh, Saudi Arabia, during winter seasons (2020–2023). Methods: NPA samples were collected from hospitalized patients presenting with fever (>38 °C) and respiratory symptoms. RNA was extracted using the QIAamp Viral RNA Kit, followed by RT-PCR for IAV (H1N1, A/H3N2) and IBV detection. Quantitative real-time PCR profiled mRNA expression of 17 cytokines/chemokines in IAV-positive (n = 65) and IBV-positive (n = 20) samples, normalized to GAPDH using the 2−ΔΔCq method. Appropriate statistical tests were applied (p < 0.05 significant). Results: Results showed 17.11% IAV positivity (7.89% A/H1N1, 9.21% A/H3N2) and 5.26% IBV. A/H3N2 predominated, increasing from 6.67% (2020/21) to 12.30% (2022/23). Males had higher IAV rates (25.88% vs. 10.00% females, p < 0.05), while IBV was higher in females (6.67% vs. 3.53%). Age-wise, 0–4 years had peak IAV (28.42%, p < 0.05); IBV peaked at 5–14 years (10.91%). IAV elicited higher mRNA expression IFN-α, IL-10, IL-13, and CCL-2 (p < 0.05); IBV showed elevated IL-1α, IL-6, and IL-33 (p < 0.05). Within IAV, A/H1N1 had higher IL-4, IL-10, IL-13, and IL-17; A/H3N2 elevated TNF-α, IL-6, IL-22, CCL-3, and CCL-4 (p < 0.05). Conclusions: These findings highlight subtype-specific inflammatory profiles and demographic disparities in Saudi Arabia, informing targeted interventions. Post-COVID resurgence underscores surveillance needs amid travel and gatherings. Insights into cytokine dynamics aid prognosis and therapeutics, emphasizing regional molecular monitoring for vaccine optimization and outbreak prevention.

## Linked entities

- **Proteins:** IFN1@ (interferon, type 1, cluster), IL10 (interleukin 10), IL13 (interleukin 13), CCL2 (C-C motif chemokine ligand 2), IL1A (interleukin 1 alpha), IL6 (interleukin 6), IL33 (interleukin 33), IL4 (interleukin 4), IL17A (interleukin 17A), TNF (tumor necrosis factor), IL22 (interleukin 22), CCL3 (C-C motif chemokine ligand 3), CCL4 (C-C motif chemokine ligand 4)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL22 (interleukin 22) [NCBI Gene 50616] {aka IL-21, IL-22, IL-D110, IL-TIF, ILTIF, TIFIL-23}, IFNA1 (interferon alpha 1) [NCBI Gene 3439] {aka IFL, IFN, IFN-ALPHA, IFN-alphaD, IFNA13, IFNA@}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CCL4 (C-C motif chemokine ligand 4) [NCBI Gene 6351] {aka ACT2, AT744.1, G-26, HC21, LAG-1, LAG1}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, CCL3 (C-C motif chemokine ligand 3) [NCBI Gene 6348] {aka G0S19-1, LD78, LD78ALPHA, MIP-1-alpha, MIP1A, SCI}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}
- **Diseases:** Influenza A and B Virus Infections (MESH:D006566), Inflammatory (MESH:D007249), influenza (MESH:D007251), Post-COVID (MESH:D000094024), fever (MESH:D005334), respiratory symptoms (MESH:D012818)
- **Species:** H1N1 subtype (serotype) [taxon 114727], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

54 references — full list in the complete paper: https://tomesphere.com/paper/PMC13025935/full.md

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Source: https://tomesphere.com/paper/PMC13025935