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Folium isatidis is a native Chinese herbaceous plant widely used for medicinal purposes for thousands of years. However, few studies have focused on the leaves of Isatis indigotica. In this report, we isolated a series of four fractions (I–IV) from Folium isatidis and explored the antiviral activity of each tested extract. The extracts were active against a panel of RNA and DNA viruses in vitro, namely influenza A virus (IAV), coxsackie virus B3 (CVB3), respiratory syncytial virus (RSV), and adenovirus type 7 (Ad-7). Oral administration of 200 mg/kg/d of fraction III in mice exerted strong antiviral effects in viral replication, accompanied by prolonged survival rate, attenuated lung tissue damage as well as significant reductions in pulmonary virus titers and lung index. Our results provide the first biochemical evidence that Folium isatidis and its extracts could be used as potential antiviral agent in the postexposure prophylaxis for multiple viral infections.

COVID-19 has posed unprecedented challenges to global public health since its outbreak. The Qing-Fei-Pai-Du decoction (QFPDD), a Chinese herbal formula, is widely used in China to treat COVID-19. It exerts an impressive therapeutic effect by inhibiting the progression from mild to critical disease in the clinic. However, the underlying mechanisms remain obscure. Both SARS-CoV-2 and influenza viruses elicit similar pathological processes. Their severe manifestations, such as acute respiratory distress syndrome (ARDS), multiple organ failure (MOF), and viral sepsis, are correlated with the cytokine storm. During flu infection, QFPDD reduced the lung indexes and downregulated the expressions of MCP-1, TNF-$\alpha$, IL-6, and IL-1$\beta$ in broncho-alveolar lavage fluid (BALF), lungs, or serum samples. The infiltration of neutrophils and inflammatory monocytes in lungs was decreased dramatically, and lung injury was ameliorated in QFPDD-treated flu mice. In addition, QFPDD also inhibited the polarization of M1 macrophages and downregulated the expressions of IL-6, TNF-$\alpha$, MIP-2, MCP-1, and IP-10, while also upregulating the IL-10 expression. The phosphorylated TAK1, IKK$\alpha$/$\beta$, and I$\kappa$B$\alpha$ and the subsequent translocation of phosphorylated p65 into the nuclei were decreased by QFPDD. These findings indicated that QFPDD reduces the intensity of the cytokine storm by inhibiting the NF-$\kappa$B signaling pathway during severe viral infections, thereby providing theoretical and experimental support for its clinical application in respiratory viral infections.

The generalized Gause model of predator-prey system is revisited with an introduction of viral infection on prey population. Stability behavior of such modified system is carried out to observe the change of dynamical behavior of the system. To substantiate the analytical results of this generalized susceptible prey, infected prey and predator population, numerical simulations of the model with specific growth and response functions are performed. Our observations suggest that the disease on prey population has a destabilizing or stabilizing effect depending on the level of force of infection and may act as a biological control for the persistence of the species.

Antiviral drug therapy that targets on boosting virus-specific immune response has become very promising in controlling the virus, especially when completely eradicating the virus from the host turns out to be difficult. Using a concrete viral infection model that incorporates the time lag needed for the expansion of immune cells, we numerically explored the joint impacts of the duration of therapy, the efficacy of the drugs and the time lag in immune expansion on immunity boosting for a single phase of therapy. Our findings reveal that a single phase of therapy can establish sustained immunity if the therapy is stopped in a suitable range of timing and large time lag in the expansion of immune cells and too strong or too weak therapy would lead to a failure in immunity boosting. Our findings may provide some insights on designing efficient and rational therapy strategies in boosting sustained immunity.

We analyze a mathematical model of predator–prey interaction where the prey population is infected with a viral disease. Infection in the prey population is assumed to follow standard incidence. The dynamical behavior of the system is studied in terms of stability aspects. To model the gestation lag of the predator species and the spatially heterogeneous characteristics of an ecological population, we incorporate the concept of diffusionally coupled delay into the system. The bifurcation behavior of the delayed homogeneous system is studied. The existence of traveling wave solutions for the delay–diffusion model is established. Numerical simulations are performed to justify analytical findings.

Abalone herpesvirus (AbHV) infection of cultured abalones Haliotis diversicolor supertexta induced acute high mortality in 2003. Years later, sporadic mortality was noted for an extended period of months, resulting in high cumulative mortality. Moribund abalones were analyzed using PCR, in situ hybridization, and histopathology, because thus far no viral particles have been observed by transmission electron microscopy. PCR using 20 primer sets, specifically designed from sequences of acute AbHV infection, failed to amplify any products from abalones suffering from chronic mortality. Subsequently, a 1406-bp sequence was amplified from chronic moribund abalones, and this sequence showed a 92% (553 bp/602 bp) homology with the gene of an AbHV Taiwan isolate (NCBI serial no. KF537536.1), suggestive of an AbHV pathotype. Histopathology of AbHV pathotype infection showed hemocyte infiltration in the lamina propia of the digestive tract, and hemocytes of various stages were evident, as well as the loss of seminal tubules in the gonad. In situ hybridization revealed that in AbHV infection, positive signals were restricted to the neural ganglia, while in AbHV pathotype infection, positive signals were observed only in the hemocytes. It appeared that the tropism of AbHV shifted from mainly neurotropic in AbHV infection to mainly hemocytotropic in abalone suffering from chronic mortality. Abalone shriveling syndrome-associated virus co-infection was detected in some of AbHV pathotype infection events. Further studies are needed to better understand the pathogenesis of AbHV pathotype affecting H. diversicolor in Taiwan.

In this paper, we consider two nonlinear models for viral infection with humoral immunity. The first model contains four compartments; uninfected target cells, actively infected cells, free virus particles and B cells. The second model is a modification of the first one by including the latently infected cells. The incidence rate, removal rate of infected cells, production rate of viruses and the latent-to-active conversion rate are given by more general nonlinear functions. We have established a set of conditions on these general functions and determined two threshold parameters for each model which are sufficient to determine the global dynamics of the models. The global asymptotic stability of all equilibria of the models has been proven by using Lyapunov theory and applying LaSalle's invariance principle. We have performed some numerical simulations for the models with specific forms of the general functions. We have shown that, the numerical results are consistent with the theoretical results.

To describe the interaction between viral infection and immune response, we establish a mathematical model with intracellular delay and investigate an optimal control problem to examine the effect of antiviral therapy. Dynamic analysis of the proposed model for the stability of equilibria and Hopf bifurcation is conducted. Theoretical results reveal that the dynamical properties are determined by both the immune-inactivated reproduction number and the immune-activated reproduction number. With the aim of minimizing the infected cells and viral load with consideration for the treatment costs, the optimal solution is discussed analytically. Numerical simulations are performed to suggest the optimal therapeutic strategy and compare the model-predicted consequences.