World Journal of
Pharmaceutical and Life Sciences

REPURPOSING OF BUDESONIDE IN HUMAN PAPILLOMAVIRUS [HPV] RELATED INFLAMMATION

*Kashid Pratiksha Vinod, Sabale Shruti Bharat, Gholap Prachi Vikas, Doifode Usha Pratap, Ghodake Aditi
Laxman, Dr. Nikunj Solanki

ABSTRACT

Human Papillomavirus (HPV) infection, particularly by high-risk types HPV-16 and HPV-18, is a major driver of cervical cancer, which ranks as the fourth most common cancer worldwide. These viruses contribute to carcinogenesis by manipulating host cellular mechanisms and immune responses to promote chronic inflammation, immune evasion, and tumor progression. The viral oncoproteins E6 and E7 disrupt tumor suppressor pathways, alter cytokine production, and interfere with immune signaling, creating a proinflammatory and immunosuppressive environment that fosters persistence of infection and malignant transformation. Addressing this complexity, systems biology and meta-analysis approaches have enabled identification of inflammation- associated gene signatures distinctive to HPV-16 and HPV-18 infected cervical cancers. These signatures allow classification of patients based on individual molecular differences, paving the way for precision medicine. The study leveraged gene signature reversal and network pharmacology to screen and repurpose anti- inflammatory drugs that target these subtype-specific inflammation pathways. Molecular docking validated the physical binding potential of these novel drug candidates to key inflammatory proteins implicated in HPV-associated carcinogenesis. Drugs such as betamethasone and methylprednisolone were identified for HPV-16, daphnetin and phenylbutazone for HPV-18, and others for both subtypes, offering tailored therapeutic options aimed at modulating chronic inflammation driving cervical cancer. Moreover, Budesonide—a glucocorticoid with potent anti-inflammatory and immunomodulatory effects— has emerged as a promising repurposed drug candidate. AI-based computational tools including machine learning, molecular docking, and network pharmacology facilitated the prediction of Budesonide’s interactions with HPV-induced inflammatory pathways and key gene targets, offering deeper molecular insight into its therapeutic potential. This integrated AI and systems biology approach highlights a shift from conventional therapies targeting HPV replication alone to combinatorial treatments that address the inflammatory microenvironment crucial for cancer progression.

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