Co-infection Model Research Articles

Analysis of a TB and HIV co-infection model under Mittag-Leffler fractal-fractional derivative

In this paper, the nonlocal operator with the Mittag-Leffler kernel is used to analyze a TB-HIV co-infection model with recurrent TB and exogenous reinfection. The non-negative invariant region and basic reproduction number of the proposed model are demonstrated. By using the Krasnoselskii fixed result, we investigate that the TB-HIV co-infection model possesses at least one solution. We look at the existence of a unique solution using Banach’s fixed point theorem. Functional analysis is used to demonstrate Ulam-Hyres stability. The numerical solution of the given model is obtained using the Adams-Bashforth technique. We illustrate the achieved results by studying the co-infection of TB and HIV for different fractional and fractal orders.

A co-infection model on TB - COVID-19 with optimal control and sensitivity analysis

COVID-19 had been declared a public health emergency by the World Health Organization in the early 2020. Since then, this deadly virus has claimed millions of lives worldwide. Amidst its chaotic spread, several other diseases have faced negligence in terms of treatment and care, of which one such chronic disease is Tuberculosis. Due to huge rise in COVID-19 cases, there had been a drastic decrease in notification of TB cases which resulted in reversal of global TB target progress. Apart from these due to the earlier co-infections of TB with SARS and MERS-CoV viruses, the TB-COVID-19 co-infection posed a severe threat in the spread of the disease. All these factors backed to be major motivation factor in development of this model. Leading with this concern, a TB - COVID-19 co-infection model is developed in this study, considering possibility of waning immunity of both diseases. Considering different epidemiological traits, an epidemiological model with 11 compartments is developed and the co-dynamics is analysed. A detailed stability and bifurcation analysis is performed for the TB only sub-model, COVID-19 only sub-model and the complete TB - COVID-19 model. Impact of key parameters namely, infection rate, waning immunity, and face mask efficacy on disease prevalence is discussed in detail. Sensitivity analysis by means of normalized forward sensitivity index of the basic reproduction number and LHS-PRCC approach is carried to provide a thorough understanding of significance of various parameters in accelerating as well as controlling the disease spread. Optimal control analysis is presented extensively, incorporating controls related to timely and improved TB treatment, and enhanced COVID-19 tests and isolation facilities to curb the spread of these infectious diseases. The simulation results obtained from each of these analyses stress on the importance of different control measures in mitigation of the diseases and are illustrated accordingly. The study suggests that in the times of a pandemic, other disease treatment and care must not be neglected, and adequate care must be taken so that mortality due to co-infection and unavailability of timely treatment can be avoided.

Backward bifurcation and optimal control in a co-infection model for SARS-CoV-2 and ZIKV

In co-infection models for two diseases, it is mostly claimed that, the dynamical behavior of the sub-models usually predict or drive the behavior of the complete models. However, under a certain assumption such as, allowing incident co-infection with both diseases, we have a different observation. In this paper, a new mathematical model for SARS-CoV-2 and Zika co-dynamics is presented which incorporates incident co-infection by susceptible individuals. It is worth mentioning that the assumption is missing in many existing co-infection models. We shall discuss the impact of this assumption on the dynamics of a co-infection model. The model also captures sexual transmission of Zika virus. The positivity and boundedness of solution of the proposed model are studied, in addition to the local asymptotic stability analysis. The model is shown to exhibit backward bifurcation caused by the disease-induced death rates and parameters associated with susceptibility to a second infection by those singly infected. Using Lyapunov functions, the disease free and endemic equilibria are shown to be globally asymptotically stable for R01, respectively. To manage the co-circulation of both infections effectively, under an endemic setting, time dependent controls in the form of SARS-CoV-2, Zika and co-infection prevention strategies are incorporated into the model. The simulations show that SARS-CoV-2 prevention could greatly reduce the burden of co-infections with Zika. Furthermore, it is also shown that prevention controls for Zika can significantly decrease the burden of co-infections with SARS-CoV-2.

Impact of saturated treatments on HIV-TB dual epidemic as a consequence of COVID-19: optimal control with awareness and treatment.

In this study, we propose an HIV-TB co-infection model by considering the treatment provision limitation induced by recent COVID-19 pandemic that impacts this dual epidemic immensely, assimilating the significance of educational attempts. We analyze the model and its submodels with single infections individually. We obtain the awareness-induced basic reproduction numbers and discuss the global stability of disease-free equilibrium when provision limitation is zero. We observe that the submodels exhibit forward as well as backward bifurcations under provision restriction. Further, we derive thresholds for resource limitations regulating the dynamical behavior of the systems while analyzing the stability of endemic equilibrium of the models with single infections. Sophisticated simulation approaches are implemented to discover the influences of provision-restricted medication and awareness on dual epidemic. Our findings convey the persistence of co-infection though the basic reproduction number is below unity, if the provision restriction remains uncurbed. An observable insight is that, in spite of having epidemic threshold less than unity and no limitation in TB treatment, co-infection relapses and persists in the population, when there is no awareness attempt. Numerical findings emphasize the urgent need of increased treatment accessibility and importance of awareness in the current situation. Moreover, an optimization problem incorporating treatment and awareness controls is formulated and solved to find the ideal strategy to manage HIV-TB co-epidemic that recommends to diminish the medical resource limitation to get the enormous impact in dominating the adversity caused by COVID-19.

On the fractional order model for HPV and Syphilis using non–singular kernel

Most dynamical systems employ the classical integer-order derivatives which yield good results. However, recent trends have shown that the application of arbitrary order derivatives, popularly known as fractional order derivatives produces better and more realistic results to a given real life scenario because they are non-local operators. In this work, a fractional order co-infection model for human papilloma virus (HPV) and Syphilis is considered and studied using the non-singular kernel derivative. With the aid of Banach and Schauder’s fixed point theorems, the existence and uniqueness of the solution is proven. The conditions for the existence and uniqueness of the solution of the model are also established. The model’s disease free equilibrium (DFE) is shown to be locally asymptotically stable when the reproduction number is below one. The fractional order model is shown to be generalized Ulam Hyers–Rassias stable, under some conditions. The predictor–corrector method with convergence of min2,1+φ was used for the numerical simulations. Simulations of the model showed that the fractional derivative greatly influenced the dynamics of both diseases and their co-infection. Furthermore, it was observed that control strategy for single infection (syphilis only prevention strategy or HPV only prevention strategy) did not result in reduction of single infection cases, instead reduces the co-infection of new cases.

Mathematical Modeling of Covid-19 and Dengue Co-Infection Dynamics in Bangladesh: Optimal Control and Data-Driven Analysis

This paper aims to explore the transmission dynamics of COVID-19 with dengue co-infection using mathematical modeling. In this study, SIR model is developed that explains the trajectory of the epidemic to boost a plan for an effective control strategy for COVID-19 in Bangladesh. The model is extended to optimal control strategies. Pontryagin’s Principle is used to establish the appropriate conditions for the existence of optimal control and the optimality system for the co-infection model. Coinfected cases were reduced with control greater than without control. Using Omicron incidence cases from 1st January – 13th April 2022, the maximum likelihood estimate of R0 with a 95% confidence interval is1.89 [ 95% CI: 1.88, 1.91]. The R0 estimated from the exponential growth method is 2.08 [95% CI: 2.07,2.09]and time-dependent estimate is 2.10[95% CI: 1.72,2.58]. The generalized logistic growth model predicted 19, 52,131 cumulative cases on day 103 (April 13, 2022), and a relatively flat curve of cumulative growth of COVID-19 cases implies a declining trend of new cases. The study also found from sensitivity analysis that, R0 is proportional to the mean generation time. This paper attempted to focus on suppressing the COVID-19 co-infections by preventing dengue and COVID-19. The results of the study show that by implementing optimal control spread of dengue and COVID-19 could be minimized. The logistic growth model suggests that the infection rate of COVID-19 is decreasing.

Mathematical Modeling and Analysis of TB and COVID-19 Coinfection

Tuberculosis (TB) and coronavirus (COVID-19) are both infectious diseases that globally continue affecting millions of people every year. They have similar symptoms such as cough, fever, and difficulty breathing but differ in incubation periods. This paper introduces a mathematical model for the transmission dynamics of TB and COVID-19 coinfection using a system of nonlinear ordinary differential equations. The well-posedness of the proposed coinfection model is then analytically studied by showing properties such as the existence, boundedness, and positivity of the solutions. The stability analysis of the equilibrium points of submodels is also discussed separately after computing the basic reproduction numbers. In each case, the disease-free equilibrium points of the submodels are proved to be both locally and globally stable if the reproduction numbers are less than unity. Besides, the coinfection disease-free equilibrium point is proved to be conditionally stable. The sensitivity and bifurcation analysis are also studied. Different simulation cases were performed to supplement the analytical results.

Pseudomonas aeruginosa polysaccharide Psl supports airway microbial community development

Pseudomonas aeruginosa dominates the complex polymicrobial cystic fibrosis (CF) airway and is a leading cause of death in persons with CF. Oral streptococcal colonization has been associated with stable CF lung function. However, no studies have demonstrated how Streptococcus salivarius, the most abundant streptococcal species found in individuals with stable CF lung disease, potentially improves lung function or becomes incorporated into the CF airway biofilm. By utilizing a two-species biofilm model to probe interactions between S. salivarius and P. aeruginosa, we discovered that the P. aeruginosa exopolysaccharide Psl promoted S. salivarius biofilm formation. Further, we identified a S. salivarius maltose-binding protein (MalE) that is required for promotion of biofilm formation both in vitro and in a Drosophila melanogaster co-infection model. Finally, we demonstrate that promotion of dual biofilm formation with S. salivarius is common among environmental and clinical P. aeruginosa isolates. Overall, our data supports a model in which S. salivarius uses a sugar-binding protein to interact with P. aeruginosa exopolysaccharide, which may be a strategy by which S. salivarius establishes itself within the CF airway microbial community.

Interacting Effects of Sea Louse (Lepeophtheirus salmonis) Infection and Formalin-Killed Aeromonas salmonicida on Atlantic Salmon Skin Transcriptome

Lepeophtheirus salmonis (sea lice) and bacterial co-infection threatens wild and farmed Atlantic salmon performance and welfare. In the present study, pre-adult L. salmonis-infected and non-infected salmon were intraperitoneally injected with either formalin-killed Aeromonas salmonicida bacterin (ASAL) or phosphate-buffered saline (PBS). Dorsal skin samples from each injection/infection group (PBS/no lice, PBS/lice, ASAL/no lice, and ASAL/lice) were collected at 24 h post-injection and used for transcriptome profiling using a 44K salmonid microarray platform. Microarray results showed no clear inflammation gene expression signatures and revealed extensive gene repression effects by pre-adult lice (2,189 down and 345 up-regulated probes) in the PBS-injected salmon (PBS/lice vs. PBS/no lice), which involved basic cellular (e.g., RNA and protein metabolism) processes. Lice repressive effects were not observed within the group of ASAL-injected salmon (ASAL/lice vs. ASAL/no lice); on the contrary, the observed skin transcriptome changes –albeit of lesser magnitude (82 up and 1 down-regulated probes)– suggested the activation in key immune and wound healing processes (e.g., neutrophil degranulation, keratinocyte differentiation). The molecular skin response to ASAL was more intense in the lice-infected (ASAL/lice vs. PBS/lice; 272 up and 11 down-regulated probes) than in the non-infected fish (ASAL/no lice vs. PBS/no lice; 27 up-regulated probes). Regardless of lice infection, the skin’s response to ASAL was characterized by the putative activation of both antibacterial and wound healing pathways. The transcriptomic changes prompted by ASAL+lice co-stimulation (ASAL/lice vs. PBS/no lice; 1878 up and 3120 down-regulated probes) confirmed partial mitigation of lice repressive effects on fundamental cellular processes and the activation of pathways involved in innate (e.g., neutrophil degranulation) and adaptive immunity (e.g., antibody formation), as well as endothelial cell migration. The qPCR analyses evidenced immune-relevant genes co-stimulated by ASAL and lice in an additive (e.g., mbl2b, bcl6) and synergistic (e.g., hampa, il4r) manner. These results provided insight on the physiological response of the skin of L. salmonis-infected salmon 24 h after ASAL stimulation, which revealed immunostimulatory properties by the bacterin with potential applications in anti-lice treatments for aquaculture. As a simulated co-infection model, the present study also serves as a source of candidate gene biomarkers for sea lice and bacterial co-infection.

A232 TUFT CELLS COORDINATE RAPID EXPULSION OF THE TAPEWORM H. DIMINUTA BUT ARE NOT REQUIRED FOR ENHANCED IMMUNITY AGAINST THE NEMATODE, H. POLYGYRUS, IN MICE PREVIOUSLY INFECTED WITH H. DIMINUTA

BackgroundThe tuft cell is an important sentinel that monitors the gut lumen and coordinates immunity against parasitic nematodes. We showed small intestinal tuft cell hyperplasia 11 days post-infection (dpi.) with the tapeworm Hymenolepis diminuta: a time when the parasite is no longer present in murine hosts. This may be a way by which the host protects itself from subsequent helminth-infections, a common phenomenon in parasite-endemic world regions. We test this supposition using Pou2f3-/- mice that lack tuft cells.AimsTo test the hypothesis that tuft cells are important in the anti-worm response in H. diminuta ( H.d.)-infected mice subsequently infected with the nematode parasite Heligosomoides polygyrus ( H.p.).MethodsMale C57BL6 and Pou2f3-/- mice (8–12 weeks) were infected with 5 H.d. cysticercoids ± 200 H.p. larvae at 10 dpi with H. diminuta (non H.p. mice - control). Upon necropsy at 24 dpi H. diminuta (i.e. 14 dpi H.p. in co-infected mice), both worms were ennumerated in small intestinal washings, H.p. granulomas examined and fecal egg counts performed. Small intestinal segments were stained for tuft (DCLK1+) and goblet cells (PAS+). As a surrogate of successful infection, IL-4 and IL-10 were measured in supernatants from concanavalin-A treated splenocytes.ResultsWild-type (WT) mice expel H. diminuta by 11 dpi and this was delayed in Pou2f3-/-mice, with worms readily detectable at 14 dpi and absent by 21 dpi. Despite the delayed expulsion, both WT and Pou2f3-/- mice showed increased splenic production of IL-4 and IL-10; however, unlike WT mice, H. diminuta-infected Pou2f3-/- mice show no increase in jejunal goblet cell numbers. Mice infected with H. diminuta displayed a degree of increased resistance to H.p.-infection defined by reduced worm and egg burdens, and increased granuloma formation in comparison to H.p.-only infected animals. In this sequential co-infection model, there were no significant differences between WT and Pou2f3-/- mice in the response to H.p.ConclusionsThe absence of tuft cells slows expulsion of H. diminuta from its non-permissive mouse host and correlates with diminished goblet cell hyperplasia. Hypothesizing that H. diminuta-evoked tuft cell hyperplasia would enhance the immune response to a subsequent infection with an unrelated nematode parasite proved incorrect. While H. diminuta-infected mice were partially protected from H.p., response was similar in WT and Pou2f3-/- mice. Thus tuft cells are important in worm detection: yet, our co-infection data suggests that other events initiated by the primary worm infection impact the outcome of subsequent infection with a different helminth and tuft cells have a limited, if any, role to play in this helminth-host-helminth interaction.Funding AgenciesCIHRNSERC, Eye’s High International doctoral scholarship

Antiretroviral therapy timing impacts latent tuberculosis infection reactivation in a Mycobacterium tuberculosis/SIV coinfection model.

Studies using the nonhuman primate model of Mycobacterium tuberculosis/simian immunodeficiency virus coinfection have revealed protective CD4+ T cell–independent immune responses that suppress latent tuberculosis infection (LTBI) reactivation. In particular, chronic immune activation rather than the mere depletion of CD4+ T cells correlates with reactivation due to SIV coinfection. Here, we administered combinatorial antiretroviral therapy (cART) 2 weeks after SIV coinfection to study whether restoration of CD4+ T cell immunity occurred more broadly, and whether this prevented reactivation of LTBI compared to cART initiated 4 weeks after SIV. Earlier initiation of cART enhanced survival, led to better control of viral replication, and reduced immune activation in the periphery and lung vasculature, thereby reducing the rate of SIV-induced reactivation. We observed robust CD8+ T effector memory responses and significantly reduced macrophage turnover in the lung tissue. However, skewed CD4+ T effector memory responses persisted and new TB lesions formed after SIV coinfection. Thus, reactivation of LTBI is governed by very early events of SIV infection. Timing of cART is critical in mitigating chronic immune activation. The potential novelty of these findings mainly relates to the development of a robust animal model of human M. tuberculosis/HIV coinfection that allows the testing of underlying mechanisms.

Mycobacterial infection aggravates Helicobacter pylori-induced gastric preneoplastic pathology by redirection of de novo induced Treg cells.

The two human pathogens Helicobacter pylori and Mycobacterium tuberculosis (Mtb) co-exist in many geographical areas of the world. Here, using a co-infection model ofH.pyloriand the Mtb relativeM.bovisbacillus Calmette-Guérin (BCG), we show that both bacteria affect the colonization and immune control of the respective other pathogen. Co-occurring M.bovis boosts gastric Th1 responses and H.pylori control and aggravates gastric immunopathology. H.pylori in the stomach compromises immune control of M.bovis in the liver and spleen. Prior antibiotic H.pylori eradication or M.bovis-specific immunization reverses the effects of H.pylori. Mechanistically, the mutual effects can be attributed to the redirection of regulatory Tcells (Treg cells) to sites of M.bovis infection. Reversal of Treg cell redirection by CXCR3 blockade restores M.bovis control. In conclusion, the simultaneous presence of both pathogens exacerbates the problems associated with each individual infection alone and should possibly be factored into treatment decisions.

Disentangling how multiple traits drive 2 strain frequencies in SIS dynamics with coinfection

A general theory for competitive dynamics among many strains at the epidemiological level is required to understand polymorphisms in virulence, transmissibility, antibiotic resistance and other biological traits of infectious agents. Mathematical coinfection models have addressed specific systems, focusing on the criteria leading to stable coexistence or competitive exclusion, however, due to their complexity and nonlinearity, analytical solutions in coinfection models remain rare. Here we study a 2-strain Susceptible-Infected-Susceptible (SIS) compartmental model with co-infection/co-colonization, incorporating five strain fitness dimensions under the same framework: variation in transmissibility, duration of carriage, pairwise susceptibilities to coinfection, coinfection duration, and transmission priority effects from mixed coinfection. Taking advantage of a singular perturbation approach, under the assumption of strain similarity, we expose how strain dynamics on a slow timescale are explicitly governed by a replicator equation which encapsulates all traits and their interplay. This allows to predict explicitly not only the final epidemiological outcome of a given 2-player competition, but moreover, their entire frequency dynamics as a direct function of their relative variation and of strain-transcending global parameters. Based on mutual invasion fitnesses, we analyze and report rigorous results on transition phenomena in the 2-strain system, strongly mediated via endemic coinfection prevalence. We show that coinfection is not always a promoter of coexistence; instead, its effect to favour or prevent polymorphism is non-monotonic and depends on the type and level of phenotypic differentiation between strains. This framework offers a deeper analytical understanding of 2-strain competitive games in coinfection, with theoretical and practical applications in epidemiology, ecology and evolution.

Global analysis of within-host SARS-CoV-2/HIV coinfection model with latency.

The coronavirus disease 2019 (COVID-19) is a respiratory disease caused by a virus called the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this paper, we analyze a within-host SARS-CoV-2/HIV coinfection model. The model is made up of eight ordinary differential equations. These equations describe the interactions between healthy epithelial cells, latently infected epithelial cells, productively infected epithelial cells, SARS-CoV-2 particles, healthy CD4^{+} T cells, latently infected CD4^{+} T cells, productively infected CD4^{+} T cells, and HIV particles. We confirm that the solutions of the developed model are bounded and nonnegative. We calculate the different steady states of the model and derive their existence conditions. We choose appropriate Lyapunov functions to show the global stability of all steady states. We execute some numerical simulations to assist the theoretical contributions. Based on our results, weak CD4^{+} T cell immunity in SARS-CoV-2/HIV coinfected patients causes an increase in the concentrations of productively infected epithelial cells and SARS-CoV-2 particles. This may lead to severe SARS-CoV-2 infection in HIV patients. This result agrees with many studies that discussed the high risk of severe infection and death in HIV patients when they get SARS-CoV-2 infection. On the other hand, increasing the death rate of infected epithelial cells during the latency period can reduce the severity of SARS-CoV-2 infection in HIV patients. More studies are needed to understand the dynamics of SARS-CoV-2/HIV coinfection and find better ways to treat this vulnerable group of patients.

Concurrent Infection With the Filarial Helminth Litomosoides sigmodontis Attenuates or Worsens Influenza A Virus Pathogenesis in a Stage-Dependent Manner.

Filarial helminths infect approximately 120 million people worldwide initiating a type 2 immune response in the host. Influenza A viruses stimulate a virulent type 1 pro-inflammatory immune response that in some individuals can cause uncontrolled immunopathology and fatality. Although coinfection with filariasis and influenza is a common occurrence, the impact of filarial infection on respiratory viral infection is unknown. The aim of this study was to determine the impact of pre-existing filarial infection on concurrent infection with influenza A virus. A murine model of co-infection was established using the filarial helminth Litomosoides sigmodontis and the H1N1 (A/WSN/33) influenza A virus (IAV). Co-infection was performed at 3 different stages of L. sigmodontis infection (larval, juvenile adult, and patency), and the impact of co-infection was determined by IAV induced weight loss and clinical signs, quantification of viral titres, and helminth counts. Significant alterations of IAV pathogenesis, dependent upon stage of infection, was observed on co-infection with L. sigmodontis. Larval stage L. sigmodontis infection alleviated clinical signs of IAV co-infection, whilst more established juvenile adult infection also significantly delayed weight loss. Viral titres remained unaltered at either infection stage. In contrast, patent L. sigmdodontis infection led to a reversal of age-related resistance to IAV infection, significantly increasing weight loss and clinical signs of infection as well as increasing IAV titre. These data demonstrate that the progression of influenza infection can be ameliorated or worsened by pre-existing filarial infection, with the outcome dependent upon the stage of filarial infection.

Malaria abrogates O'nyong-nyong virus pathologies by restricting virus infection in nonimmune cells.

O'nyongnyong virus (ONNV) is a re-emerging alphavirus previously known to be transmitted by main malaria vectors, thus suggesting the possibility of coinfections with arboviruses in co-endemic areas. However, the pathological outcomes of such infections remain unknown. Using murine coinfection models, we demonstrated that a preexisting blood-stage Plasmodium infection suppresses ONNV-induced pathologies. We further showed that suppression of viremia and virus dissemination are dependent on Plasmodium-induced IFNγ and are associated with reduced infection of CD45- cells at the site of virus inoculation. We further proved that treatment with IFNγ or plasma samples from Plasmodium vivax-infected patients containing IFNγ are able to restrict ONNV infection in human fibroblast, synoviocyte, skeletal muscle, and endothelial cell lines. Mechanistically, the role of IFNγ in restricting ONNV infection was confirmed in in vitro infection assays through the generation of an IFNγ receptor 1 α chain (IFNγR1)-deficient cell line.

HIV/AIDS-Pneumonia Codynamics Model Analysis with Vaccination and Treatment.

In this paper, we proposed and analyzed a realistic compartmental mathematical model on the spread and control of HIV/AIDS-pneumonia coepidemic incorporating pneumonia vaccination and treatment for both infections at each infection stage in a population. The model exhibits six equilibriums: HIV/AIDS only disease-free, pneumonia only disease-free, HIV/AIDS-pneumonia coepidemic disease-free, HIV/AIDS only endemic, pneumonia only endemic, and HIV/AIDS-pneumonia coepidemic endemic equilibriums. The HIV/AIDS only submodel has a globally asymptotically stable disease-free equilibrium if ℛ1 < 1. Using center manifold theory, we have verified that both the pneumonia only submodel and the HIV/AIDS-pneumonia coepidemic model undergo backward bifurcations whenever ℛ2 < 1 and ℛ3 = max{ℛ1, ℛ2} < 1, respectively. Thus, for pneumonia infection and HIV/AIDS-pneumonia coinfection, the requirement of the basic reproduction numbers to be less than one, even though necessary, may not be sufficient to completely eliminate the disease. Our sensitivity analysis results demonstrate that the pneumonia disease transmission rate β2 and the HIV/AIDS transmission rate β1 play an important role to change the qualitative dynamics of HIV/AIDS and pneumonia coinfection. The pneumonia infection transmission rate β2 gives rises to the possibility of backward bifurcation for HIV/AIDS and pneumonia coinfection if ℛ3 = max{ℛ1, ℛ2} < 1, and hence, the existence of multiple endemic equilibria some of which are stable and others are unstable. Using standard data from different literatures, our results show that the complete HIV/AIDS and pneumonia coinfection model reproduction number is ℛ3 = max{ℛ1, ℛ2} = max{1.386, 9.69 } = 9.69 at β1 = 2 and β2 = 0.2 which shows that the disease spreads throughout the community. Finally, our numerical simulations show that pneumonia vaccination and treatment against disease have the effect of decreasing pneumonia and coepidemic disease expansion and reducing the progression rate of HIV infection to the AIDS stage.

Transcriptome Analysis of Atlantic Salmon (Salmo salar) Skin in Response to Sea Lice and Infectious Salmon Anemia Virus Co-Infection Under Different Experimental Functional Diets.

Sea lice (Lepeophtheirus salmonis) are ectoparasitic copepods that cause significant economic loss in marine salmoniculture. In commercial salmon farms, infestation with sea lice can enhance susceptibility to other significant pathogens, such as the highly contagious infectious salmon anemia virus (ISAv). In this study, transcriptomic analysis was used to evaluate the impact of four experimental functional feeds (i.e. 0.3% EPA/DHA+high-ω6, 0.3% EPA/DHA+high-ω6+immunostimulant (IS), 1% EPA/DHA+high-ω6, and 1% EPA/DHA+high-ω3) on Atlantic salmon (Salmo salar) during a single infection with sea lice (L. salmonis) and a co-infection with sea lice and ISAv. The overall objectives were to compare the transcriptomic profiles of skin between lice infection alone with co-infection groups and assess differences in gene expression response among animals with different experimental diets. Atlantic salmon smolts were challenged with L. salmonis following a 28-day feeding trial. Fish were then challenged with ISAv at 18 days post-sea lice infection (dpi), and maintained on individual diets, to establish a co-infection model. Skin tissues sampled at 33 dpi were subjected to RNA-seq analysis. The co-infection’s overall survival rates were between 37%-50%, while no mortality was observed in the single infection with lice. With regard to the infection status, 756 and 1303 consensus differentially expressed genes (DEGs) among the four diets were identified in “lice infection vs. pre-infection” and “co-infection vs. pre-infection” groups, respectively, that were shared between the four experimental diets. The co-infection groups (co-infection vs. pre-infection) included up-regulated genes associated with glycolysis, the interferon pathway, complement cascade activity, and heat shock protein family, while the down-regulated genes were related to antigen presentation and processing, T-cell activation, collagen formation, and extracellular matrix. Pathway enrichment analysis conducted between infected groups (lice infection vs. co-infection) resulted in several immune-related significant GO terms and pathways unique to this group, such as “autophagosome”, “cytosolic DNA-sensing pathway” and “response to type I interferons”. Understanding how experimental functional feeds can impact the host response and the trajectory of co-infections will be an essential step in identifying efficacious intervention strategies that account for the complexities of disease in open cage culture.

Global stability of HIV/HTLV co-infection model with CTL-mediated immunity

&lt;p style='text-indent:20px;'&gt;Mathematical modeling of human immunodeficiency virus (HIV) and human T-lymphotropic virus type Ⅰ (HTLV-I) mono-infections has received considerable attention during the last decades. These two viruses share the same way of transmission between individuals; through direct contact with certain contaminated body fluids. Therefore, a person can be co-infected with both viruses. In the present paper, we construct and analyze a new HIV/HTLV-I co-infection model under the effect of Cytotoxic T lymphocytes (CTLs) immune response. The model describes the interaction between susceptible CD&lt;inline-formula&gt;&lt;tex-math id="M1"&gt;\begin{document}$ 4^{+} $\end{document}&lt;/tex-math&gt;&lt;/inline-formula&gt;T cells, silent HIV-infected cells, active HIV-infected cells, silent HTLV-infected cells, Tax-expressing (active) HTLV-infected cells, free HIV particles, HIV-specific CTLs and HTLV-specific CTLs. The HIV can spread by two routes of transmission, virus-to-cell (VTC) and cell-to-cell (CTC). Both active and silent HIV-infected cells can infect the susceptible CD&lt;inline-formula&gt;&lt;tex-math id="M2"&gt;\begin{document}$ 4^{+} $\end{document}&lt;/tex-math&gt;&lt;/inline-formula&gt;T cells by CTC mechanism. On the other side, HTLV-I has only one mode of transmission via direct cell-to-cell contact. The well-posedness of the model is established by showing that the solutions of the model are nonnegative and bounded. We calculate all possible equilibria and define the key threshold parameters which govern the existence and stability of all equilibria of the model. We explore the global asymptotic stability of all equilibria by utilizing Lyapunov function and LaSalle's invariance principle. We have discussed the influence of CTL immune response on the co-infection dynamics. We have presented numerical simulations to justify the applicability and effectiveness of the theoretical results. In addition, we evaluate the effect of HTLV-I infection on the HIV dynamics and vice versa.&lt;/p&gt;

Global dynamics of IAV/SARS-CoV-2 coinfection model with eclipse phase and antibody immunity.

Coronavirus disease 2019 (COVID-19) and influenza are two respiratory infectious diseases of high importance widely studied around the world. COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), while influenza is caused by one of the influenza viruses, A, B, C, and D. Influenza A virus (IAV) can infect a wide range of species. Studies have reported several cases of respiratory virus coinfection in hospitalized patients. IAV mimics the SARS-CoV-2 with respect to the seasonal occurrence, transmission routes, clinical manifestations and related immune responses. The present paper aimed to develop and investigate a mathematical model to study the within-host dynamics of IAV/SARS-CoV-2 coinfection with the eclipse (or latent) phase. The eclipse phase is the period of time that elapses between the viral entry into the target cell and the release of virions produced by that newly infected cell. The role of the immune system in controlling and clearing the coinfection is modeled. The model simulates the interaction between nine compartments, uninfected epithelial cells, latent/active SARS-CoV-2-infected cells, latent/active IAV-infected cells, free SARS-CoV-2 particles, free IAV particles, SARS-CoV-2-specific antibodies and IAV-specific antibodies. The regrowth and death of the uninfected epithelial cells are considered. We study the basic qualitative properties of the model, calculate all equilibria, and prove the global stability of all equilibria. The global stability of equilibria is established using the Lyapunov method. The theoretical findings are demonstrated via numerical simulations. The importance of considering the antibody immunity in the coinfection dynamics model is discussed. It is found that without modeling the antibody immunity, the case of IAV and SARS-CoV-2 coexistence will not occur. Further, we discuss the effect of IAV infection on the dynamics of SARS-CoV-2 single infection and vice versa.