On the fractional SIRD mathematical model and control for the transmission of COVID-19: The first and the second waves of the disease in Iran and Japan.

In this paper, a fractional-order SIRD mathematical model is presented with Caputo derivative for the transmission of COVID-19 between humans. We calculate the steady-states of the system and discuss their stability. We also discuss the existence and uniqueness of a non-negative solution for the system under study.

A mathematical model for COVID-19 transmission by using the Caputo fractional derivative.

We present a mathematical model for the transmission of COVID-19 by the Caputo fractional-order derivative. We calculate the equilibrium points and the reproduction number for the model and obtain the region of the feasibility of system. By fixed point theory, we prove the existence of a unique solution.

SEIR epidemic model for COVID-19 transmission by Caputo derivative of fractional order.

We provide a SEIR epidemic model for the spread of COVID-19 using the Caputo fractional derivative. The feasibility region of the system and equilibrium points are calculated and the stability of the equilibrium points is investigated. We prove the existence of a unique solution for the model by using fixed point theory.

A fractional differential equation model for the COVID-19 transmission by using the Caputo-Fabrizio derivative.

We present a fractional-order model for the COVID-19 transmission with Caputo-Fabrizio derivative. Using the homotopy analysis transform method (HATM), which combines the method of homotopy analysis and Laplace transform, we solve the problem and give approximate solution in convergent series. We prove the existence of a unique solution and the stability of the iteration approach by using fixed point theory.

HIV antiretroviral exposure in pregnancy induces detrimental placenta vascular changes that are rescued by progesterone supplementation.

Adverse birth outcomes are common in HIV-positive pregnant women receiving combination antiretroviral therapy (cART), especially when cART is initiated in early pregnancy. The mechanisms remain poorly understood. Using a mouse model we demonstrate that protease inhibitor based-cART exposure beginning on day 1 of pregnancy was associated with a pro-angiogenic/pro-branching shift in the placenta driven by lower Flt-1 levels and higher Gcm-1 expression.

Low Prolactin and High 20-α-Hydroxysteroid Dehydrogenase Levels Contribute to Lower Progesterone Levels in HIV-Infected Pregnant Women Exposed to Protease Inhibitor-Based Combination Antiretroviral Therapy.

Background: It has been reported that pregnant women receiving protease inhibitor (PI)-based combination antiretroviral therapy (cART) have lower levels of progesterone, which put them at risk of adverse birth outcomes, such as low birth weight. We sought to understand the mechanisms involved in this decline in progesterone level.

Methods: We assessed plasma levels of progesterone, prolactin, and lipids and placental expression of genes involved in progesterone metabolism in 42 human immunodeficiency virus (HIV)-infected and 31 HIV-uninfected pregnant women.

HIV protease inhibitor use during pregnancy is associated with decreased progesterone levels, suggesting a potential mechanism contributing to fetal growth restriction.

Background: Protease inhibitor (PI)-based combination antiretroviral therapy (cART) is administered during pregnancy to prevent perinatal human immunodeficiency virus (HIV) transmission. However, PI use has been associated with adverse birth outcomes, including preterm delivery and small-for-gestational-age (SGA) births. The mechanisms underlying these outcomes are unknown.

Some existence results on nonlinear fractional differential equations.

In this paper, by using fixed-point methods, we study the existence and uniqueness of a solution for the nonlinear fractional differential equation boundary-value problem D(α)u(t)=f(t,u(t)) with a Riemann-Liouville fractional derivative via the different boundary-value problems u(0)=u(T), and the three-point boundary condition u(0)=β(1)u(η) and u(T)=β(2)u(η), where T>0, t∈I=[0,T], 0<α<1, 0<η View Article and Find Full Text PDF

Pharmacological inhibition of feline immunodeficiency virus (FIV).

Feline immunodeficiency virus (FIV) is a member of the retroviridae family of viruses and causes an acquired immunodeficiency syndrome (AIDS) in domestic and non-domestic cats worldwide. Genome organization of FIV and clinical characteristics of the disease caused by the virus are similar to those of human immunodeficiency virus (HIV). Both viruses infect T lymphocytes, monocytes and macrophages, and their replication cycle in infected cells is analogous.

Marek's disease virus influences the expression of genes associated with IFN-gamma-inducible MHC class II expression.

Chickens infected with Marek's disease virus (MDV) become lifelong carriers regardless of their susceptibility to clinical disease. Therefore various viral immune-evasive mechanisms must play a role in MDV-host interactions. MDV has previously been shown to influence the expression of major histocompatibility complex (MHC) class II molecules.

Characterization of host responses against a recombinant fowlpox virus-vectored vaccine expressing the hemagglutinin antigen of an avian influenza virus.

There currently are commercial fowlpox virus (FPV)-vectored vaccines for use in chickens, including TROVAC-AIV H5, which expresses the hemagglutinin (HA) antigen of an avian influenza virus and can confer immunity against avian influenza in chickens. Despite the use of recombinant FPV (rFPV) for vaccine delivery, very little is known about the immune responses generated by these viruses in chickens. The present study was designed to investigate host responses to rFPV in vivo and in vitro.

The lactate dehydrogenase-elevating virus capsid protein is a nuclear-cytoplasmic protein.

Arteriviruses replicate in the cytoplasm and do not require the nucleus function for virus multiplication in vitro. However, nucleocapsid (N) protein of two arteriviruses, porcine reproductive respiratory syndrome virus and equine arteritis virus, has been observed to localize in the nucleus and nucleolus of virus-infected and N-gene-transfected cells in addition to their normal cytoplasmic distribution. In the present study, the N protein of lactate dehydrogenase-elevating virus (LDV) of mice was examined for nuclear localization.