Since the SARS-CoV-2 outbreak, pharmaceutical companies and researchers worldwide have worked hard to develop vaccines and drugs to end the SARS-CoV-2 pandemic. The potential pathogen responsible for Coronavirus Disease 2019 (COVID-19), SARS-CoV-2, belongs to a novel lineage of beta coronaviruses in the subgenus arbovirus. Antiviral drugs, convalescent plasma, monoclonal antibodies, and vaccines are effective treatments for SARS-CoV-2 and are beneficial in preventing infection. Numerous studies have already been conducted using the genome sequence of SARS-CoV-2 in comparison with that of other SARS-like viruses, and numerous treatments/prevention measures are currently undergoing or have already undergone clinical trials. We summarize these studies in depth in the hopes of highlighting some key details that will help us to better understand the viral origin, epidemiology, and treatments of the virus.

This review delves into the historical context, current epidemiological landscape, genomics, and pathobiology of monkeypox virus (MPXV). Furthermore, it elucidates the present vaccination status and strategies to curb the spread of monkeypox. Monkeypox, caused by the Orthopoxvirus known as MPXV, is a zoonotic ailment. MPXV can be transmitted from person to person through respiratory droplets during prolonged face‐to‐face interactions. While many cases of monkeypox are self‐limiting, vulnerable groups such as young children, pregnant women, and immunocompromised individuals may experience severe manifestations. Diagnosis predominantly relies on clinical presentations, complemented by laboratory techniques like RT‐PCR. Although treatment is often not required, severe cases necessitate antiviral medications like tecovirimat, cidofovir, and brincidofovir. Vaccination, particularly using the smallpox vaccine, has proven instrumental in outbreak control, exhibiting an efficacy of at least 85% against mpox as evidenced by data from Africa. Mitigating transmission requires measures like wearing surgical masks, adequately covering skin lesions, and avoiding handling wild animals.

Brucella is an intracellular parasitic bacterium with a wide host range. It can infect terrestrial mammals, including domestic animals such as cattle and sheep, as well as wild animals like elk and bison. It also infects marine mammals, and amphibians. These diverse hosts form the basis for the classification of Brucella into different species. It can invade multiple cell types, including human cells such as monocytes/macrophages, dendritic cells (DCs), and trophoblasts; primary animal cells such as murine and bovine macrophages, and canine trophoblasts; and established cell lines such as HeLa and Vero cells. Among these, macrophages, DCs, and trophoblasts are the main target cells. Brucella employs a variety of strategies to evade host defenses: (1) obstruction of pattern recognition receptors; (2) formation of replicative Brucella-containing vacuoles following entry into host cells; (3) suppression of innate immunity through manipulation of autophagy, endoplasmic reticulum stress, inflammasomes, pyroptosis, apoptosis, ferroptosis, and pathways including cGAS-STING; and (4) inhibition of adaptive immunity through reduced antigen presentation. Compromised innate and adaptive immunity allows Brucella to replicate and survive within host cells, leading to chronic infections that are difficult to eradicate. Notably, Brucella suppresses host immunity by producing virulence factors that inhibit cytokine release and antigen presentation, and that interfere with critical signaling pathways such as programed cell death, ultimately downregulating both innate and adaptive immune responses. Collectively, these features have made the development of treatments and vaccines for brucellosis particularly challenging. While a better understanding of virulence factors is key to the effective prevention and control of brucellosis, many pathogenic mechanisms remain unclear. In this systematic review, we focus on the interactions between Brucella and the host immune system. Specifically, we examine the roles of the following factors in Brucella infection: lipopolysaccharides, flagella, the type IV secretion system (T4SS), effector proteins secreted by the T4SSs and non-T4SS, outer membrane proteins, phosphatidylcholine, mechanisms of intracellular survival, pathogen-associated molecular patterns, pattern recognition receptors, subversion of selective autophagy, endoplasmic reticulum stress pathways, inflammasomes, pyroptosis, apoptosis, ferroptosis, and the cGAS-STING pathway. We anticipate that this overview will offer new insights for research and development into drugs and vaccines for brucellosis.

Signal peptides (SPs) are short amino acid sequences located at the N-terminus of nascent proteins and are widely present across various life forms. They play crucial roles in protein synthesis, transmembrane transport, and intracellular signal transduction. With the rapid advancement of bioinformatics, studies have revealed that the functions of SPs are far more complex than previously understood. In recombinant protein expression systems, the rational design and optimization of SPs are essential for enhancing the expression efficiency and secretion level of exogenous proteins. Meanwhile, the application value of SPs in vaccine development has attracted increasing attention. This review summarizes the structural characteristics, functional mechanisms, and applications of SPs in recombinant protein production and SP-based vaccines. It also discusses their biological roles, the significance of engineering optimization strategies, and the current challenges, aiming to provide theoretical support and practical guidance for improving recombinant protein yield and advancing SP-based vaccine development.