The advent of advanced molecular technologies, particularly the widespread use of next-generation sequencing (NGS), has revolutionized the life sciences research landscape. NGS, characterized by high throughput, specificity, and sensitivity, offers a superior alternative to traditional detection methods, particularly in the context of viral pandemics and emerging infectious diseases. It has proven indispensable not only in identifying novel therapeutic targets but also in monitoring viral resistance. This review provides a comprehensive analysis of NGS applications in infectious diseases and pathogenic microorganisms, with an emphasis on its role in rapid pathogen detection, accurate identification, interspecies transmission tracking, and resistance profiling. Through the integration of these insights, the review offers a forward-looking perspective on emerging trends and challenges, highlighting the transformative impact of these technologies on the understanding and management of infectious diseases.

Liver fibrosis, resulting from chronic liver damage and characterized by the accumulation of extracellular matrix (ECM) proteins, is a characteristic of most types of chronic liver diseases. The activation of hepatic stellate cells (HSC) is considered an essential pathological hallmark in liver fibrosis. Although nitric oxide (NO) can effectively induce HSC apoptosis, the systemic administration of NO is ineffective and may cause severe complications such as hypotension. To overcome this limitation, nanoparticles were designed to target HSCs and release NO locally under the exposure of near infrared light (NIR). To achieve this, upconversion nanoparticle (UCNP) cores were enveloped in mesoporous silica shells (UCNP@mSiO₂), which were modified with hyaluronic acid (HA-UCNP@mSiO₂) and Roussin’s black salt (RBS). HA molecules recognize and bind to CD44 proteins, which are overexpressed on activated HSCs. Under exposure to a 980-nm NIR laser, the UCNP cores convert the 980-nm wavelength into ultraviolet (UV) light, which then energizes the RBS (NO donors), resulting in an efficient release of NO inside of the HSCs. Once released, NO triggers HSC apoptosis and reverses the liver fibrosis. This targeted and controlled release method provides the theoretical and experimental basis for novel therapeutic approaches to treat hepatic fibrosis.