Human Immunodeficiency Virus Dynamics Research Articles

Modeling virus-stimulated proliferation of CD4[formula omitted] T-cell, cell-to-cell transmission and viral loss in HIV infection dynamics

Human immunodeficiency virus (HIV) can persist in infected individuals despite prolonged antiretroviral therapy and it may spread through two modes: virus-to-cell and cell-to-cell transmissions. Understanding viral infection dynamics is pivotal for elucidating HIV pathogenesis. In this study, we incorporate the loss term of virions, and both virus-to-cell and cell-to-cell infection modes into a within-host HIV model, which also takes into consideration the proliferation of healthy target cells stimulated by free viruses. By constructing suitable Lyapunov function and applying geometric methods, we establish global stability results of the infection free equilibrium and the infection persistent equilibrium, respectively. Our findings highlight the crucial role of the basic reproduction number in the threshold dynamics. Moreover, we use the loss rate of virions as the bifurcation parameter to investigate stability switches of the positive equilibrium, local Hopf bifurcation, and its global continuation. Numerical simulations validate our theoretical results, revealing rich viral dynamics including backward bifurcation, saddle–node bifurcation, and bistability phenomenon in the sense that the infection free equilibrium and a limit cycle are both locally asymptotically stable. These insights contribute to a deeper understanding of HIV dynamics and inform the development of effective therapeutic strategies.

The Intersection of HIV and Social Determinants of Health: A Comprehensive Review

The Human Immunodeficiency Virus (HIV) epidemic remained a profound global health challenge, significantly impacting marginalized and underserved populations. While advances in antiretroviral therapy (ART) and prevention strategies have transformed HIV into a manageable chronic condition, the epidemic’s persistence is deeply intertwined with social determinants of health (SDOH). This comprehensive review examined the intersection of HIV and SDOH, highlighting how factors such as poverty, education, gender inequality, healthcare access, and stigma influenced HIV vulnerability and outcomes. Through a synthesis of current research and data, and utilizing a methodology that includes a systematic review of peer-reviewed literature and global health reports, the review underscored the critical role of SDOH in shaping HIV dynamics. It explored regional and population-based disparities, discussed innovations and interventions in HIV prevention and treatment, and proposed strategies to address these underlying determinants. Understanding and addressing the intersection of HIV and SDOH is crucial for developing more effective, equitable, and sustainable HIV prevention and treatment approaches, ultimately advancing global health equity and moving closer to ending the HIV epidemic as a public health threat. Keywords: Social Determinants of Health (SDOH), HIV Prevention, Economic Inequality, Stigma and Discrimination, Innovative Interventions.

Transmission Dynamics of Adolescent HIV is Very Different from Adults: A Longitudinal Study from India.

Behavioral risk factors in adolescents make them vulnerable to human immunodeficiency virus (HIV). Although it is dissimilar to adults, adolescent HIV is less studied. This study aimed to determine various socio-demographic attributes and transmission dynamics associated with adolescent HIV in order to comment on how they differ from the overall epidemiology of HIV. A record-based, comparative study was conducted using data from adolescents (ALHIV) and adults registered in all HIV centers across the Indian state of West Bengal over four years. The socio-demographic profile and modes of HIV transmission were studied. Transmission dynamics were compared between adolescent and non-adolescent beneficiaries, as well as male and female HIV-positive adolescents. The association of adolescent HIV burden with child marriage and adolescent pregnancy rates was also tested. More than 50% of AL-HIVs were students. While heterosexuality (87.17%) was the commonest route of HIV transmission in adults, parent-to-child transmission (PTCT) (51.69%) and blood transfusions (12.86%) were major routes in AL-HIVs; also, they were significantly more prone to get infected through these routes. PTCT was significantly lower, and transmission by needle syringes was higher in male adolescents than in their female counterparts. Districts with a higher prevalence of child marriage and adolescent pregnancy had a significantly higher burden of AL-HIV. The transmission dynamics of adolescent HIV are largely different from those of adults, with PTCT and sociocultural issues playing significant roles. It is, therefore, essential to design targeted interventions to tackle the unique challenges of HIV in adolescents for more effective and comprehensive campaigns against the pandemic.

Modelling Role of Protective and Nonprotective HLA Allele Inducing Different HIV Infection Outcomes

Human immunodeficiency virus (HIV) infects CD4+ cells and causes progressive immune function failure, and CD8+ cells lyse infected CD4+ cell via recognising peptide presented by human leukocyte antigens (HLA). Variations in HLA allele lead to observed different HIV infection outcomes. Within-host HIV dynamics involves virus replication within infected cells and lysing of infected cells by CD8+ cells, but how variations in HLA alleles determine different infection outcomes was far from clear. Here, we used mathematical modelling and parameter inference with a new analysis of published virus inhibition assay data to estimate CD8+ cell lysing efficiency, and found that lysing efficiency fall in the gap between low bound (0.1–0.2 day−1 (Elemans et al. in PLoS Comput Biol 8(2):e1002381, 2012)) and upper boundary (6.5–8.4 day−1 (Wick et al. in J Virol 79(21):13579–13586, 2005)). Our outcomes indicate that both lysing efficiency and viral inoculum size jointly determine observed different infection outcomes. Low lysing rate associated with non-protective HLA alleles leads to monostable viral kinetic to high viral titre and oscillatory viral kinetics. High lysing rate associated with protective HLA alleles leads monostable viral kinetic to low viral titre and bistable viral kinetics; at a specific interval of CD8+ cell counts, small viral inoculum sizes are inhibited but not large viral inoculum sizes remain infectious. Further, with CD8+ cell recruitment, HIV kinetics always exhibit oscillatory kinetics, but lysing rate is negatively correlated with range of CD8+ cell count. Our finding highlights role of HLA allele determining different infection outcomes, thereby providing a potential mechanistic explanation for observed good and bad HIV infection outcomes induced by protective HLA allele.

Stability and backward bifurcation for an HIV model with macrophages and CD4+T cells with latent reservoirs

Human immunodeficiency virus (HIV) primarily attacks CD4+ T cells but can also attack macrophage and dendritic cells leading to AIDS disease. Antiretroviral therapies are unavoidable to treat patients with HIV. However, the existing therapies failed in eliminating viral particles in infected patients. The establishment of a latency state in these patients could play a major role in this failure. To better understand the impact of different drug therapies on HIV dynamics, we propose an in-host model describing the dynamics of HIV and its interaction with both CD4+T and macrophage cells. This model incorporates the CD4+T latent reservoir as well. Results on the positivity, boundedness, and stability of solutions are shown. Furthermore, the basic reproduction number R0 is obtained using the next generation-matrix method. It is shown that the model is locally asymptotically stable at disease-free equilibrium (DFE) when the basic reproduction number R0<1. Moreover, the model exhibits either forward or backward bifurcation when R0=1. The global asymptotic stability of equilibria is investigated using suitable Lyapunov functions. To study the impact of our model parameters on the model dynamics, a sensitivity analysis is performed using the partial rank correlation coefficient method and the Latin hypercube sampling. Finally, numerical simulations are carried out to assess several drug therapy strategies to reduce HIV infection and improve health outcomes for HIV infected patients.

A novel simulation-based analysis of a stochastic HIV model with the time delay using high order spectral collocation technique

The economic impact of Human Immunodeficiency Virus (HIV) goes beyond individual levels and it has a significant influence on communities and nations worldwide. Studying the transmission patterns in HIV dynamics is crucial for understanding the tracking behavior and informing policymakers about the possible control of this viral infection. Various approaches have been adopted to explore how the virus interacts with the immune system. Models involving differential equations with delays have become prevalent across various scientific and technical domains over the past few decades. In this study, we present a novel mathematical model comprising a system of delay differential equations to describe the dynamics of intramural HIV infection. The model characterizes three distinct cell sub-populations and the HIV virus. By incorporating time delay between the viral entry into target cells and the subsequent production of new virions, our model provides a comprehensive understanding of the infection process. Our study focuses on investigating the stability of two crucial equilibrium states the infection-free and endemic equilibriums. To analyze the infection-free equilibrium, we utilize the LaSalle invariance principle. Further, we prove that if reproduction is less than unity, the disease free equilibrium is locally and globally asymptotically stable. To ensure numerical accuracy and preservation of essential properties from the continuous mathematical model, we use a spectral scheme having a higher-order accuracy. This scheme effectively captures the underlying dynamics and enables efficient numerical simulations.

Human immunodeficiency virus dynamics in secondary lymphoid tissues and the evolution of cytotoxic T lymphocyte escape mutants.

In secondary lymphoid tissues, human immunodeficiency virus (HIV) can replicate in both the follicular and extrafollicular compartments. Yet, virus is concentrated in the follicular compartment in the absence of antiretroviral therapy, in part due to the lack of cytotoxic T lymphocyte (CTL)-mediated activity there. CTLs home to the extrafollicular compartment, where they can suppress virus load to relatively low levels. We use mathematical models to show that this compartmentalization can explain seemingly counter-intuitive observations. First, it can explain the observed constancy of the viral decline slope during antiviral therapy in the peripheral blood, irrespective of the presence of CTL in Simian Immunodeficiency Virus (SIV)-infected macaques, under the assumption that CTL-mediated lysis significantly contributes to virus suppression. Second, it can account for the relatively long times it takes for CTL escape mutants to emerge during chronic infection even if CTL-mediated lysis is responsible for virus suppression. The reason is the heterogeneity in CTL activity and the consequent heterogeneity in selection pressure between the follicular and extrafollicular compartments. Hence, to understand HIV dynamics more thoroughly, this analysis highlights the importance of measuring virus populations separately in the extrafollicular and follicular compartments rather than using virus load in peripheral blood as an observable; this hides the heterogeneity between compartments that might be responsible for the particular patterns seen in the dynamics and evolution of the HIV in vivo.

A Bayesian approach for mixed effects state-space models under skewness and heavy tails.

Human immunodeficiency virus (HIV) dynamics have been the focus of epidemiological and biostatistical research during the past decades to understand the progression of acquired immunodeficiency syndrome (AIDS) in the population. Although there are several approaches for modeling HIV dynamics, one of the most popular is based on Gaussian mixed-effects models because of its simplicity from the implementation and interpretation viewpoints. However, in some situations, Gaussian mixed-effects models cannot (a) capture serial correlation existing in longitudinal data, (b) deal with missing observations properly, and (c) accommodate skewness and heavy tails frequently presented in patients' profiles. For those cases, mixed-effects state-space models (MESSM) become a powerful tool for modeling correlated observations, including HIV dynamics, because of their flexibility in modeling the unobserved states and the observations in a simple way. Consequently, our proposal considers an MESSM where the observations' error distribution is a skew-t. This new approach is more flexible and can accommodate data sets exhibiting skewness and heavy tails. Under the Bayesian paradigm, an efficient Markov chain Monte Carlo algorithm is implemented. To evaluate the properties of the proposed models, we carried out some exciting simulation studies, including missing data in the generated data sets. Finally, we illustrate our approach with an application in the AIDS Clinical Trial Group Study 315 (ACTG-315) clinical trial dataset.

Dynamic analysis of a latent HIV infection model with CTL immune and antibody responses

This paper develops a mathematical model to investigate the Human Immunodeficiency Virus (HIV) infection dynamics. The model includes two transmission modes (cell-to-cell and cell-free), two adaptive immune responses (cytotoxic T-lymphocyte (CTL) and antibody), a saturated CTL immune response, and latent HIV infection. The existence and local stability of equilibria are fully characterized by four reproduction numbers. Through sensitivity analyses, we assess the partial rank correlation coefficients of these reproduction numbers and identify that the infection rate via cell-to-cell transmission, the number of new viruses produced by each infected cell during its life cycle, the clearance rate of free virions, and immune parameters have the greatest impact on the reproduction numbers. Additionally, we compare the effects of immune stimulation and cell-to-cell spread on the model’s dynamics. The findings highlight the significance of adaptive immune responses in increasing the population of uninfected cells and reducing the numbers of latent cells, infected cells, and viruses. Furthermore, cell-to-cell transmission is identified as a facilitator of HIV transmission. The analytical and numerical results presented in this study contribute to a better understanding of HIV dynamics and can potentially aid in improving HIV management strategies.

When Bacteria and Viruses Collide: A Tale of Chlamydia trachomatis and Sexually Transmitted Viruses.

The global incidence of sexually transmitted infections (STIs) remains high, with the World Health Organization (WHO) estimating that over 1 million people acquire STIs daily. STIs can lead to infertility, pregnancy complications, and cancers. Co-infections with multiple pathogens are prevalent among individuals with an STI and can lead to heightened infectivity and more severe clinical manifestations. Chlamydia trachomatis (CT) is the most reported bacterial STI worldwide in both men and women, and several studies have demonstrated co-infection of CT with viral and other bacterial STIs. CT is a gram-negative bacterium with a unique biphasic developmental cycle including infectious extracellular elementary bodies (EBs) and metabolically active intracellular reticulate bodies (RBs). The intracellular form of this organism, RBs, has evolved mechanisms to persist for long periods within host epithelial cells in a viable but non-cultivable state. The co-infections of CT with the most frequently reported sexually transmitted viruses: human immunodeficiency virus (HIV), human papillomavirus (HPV), and herpes simplex virus (HSV) have been investigated through in vitro and in vivo studies. These research studies have made significant strides in unraveling the intricate interactions between CT, these viral STIs, and their eukaryotic host. In this review, we present an overview of the epidemiology of these co-infections, while specifically delineating the underlying mechanisms by which CT influences the transmission and infection dynamics of HIV and HSV. Furthermore, we explore the intricate relationship between CT and HPV infection, with a particular emphasis on the heightened risk of cervical cancer. By consolidating the current body of knowledge, we provide valuable insights into the complex dynamics and implications of co-infection involving CT and sexually transmitted viruses.

Dynamical behavior of a stochastic HIV model with logistic growth and Ornstein-Uhlenbeck process

In this paper, we investigate a stochastic human immunodeficiency virus (HIV) model with logistic growth and Ornstein-Uhlenbeck process, which is used to describe the pathogenesis and transmission dynamics of HIV in the population. We first validate that the stochastic system has a unique global solution with any initial value. Then we use a novel Lyapunov function method to establish sufficient conditions for the existence of a stationary distribution of the system, which shows the coexistence of all CD4+ T cells and free viruses. Especially, under some mild conditions which are used to ensure the local asymptotic stability of the quasi-chronic infection equilibrium of the stochastic system, we obtain the specific expression of covariance matrix in the probability density around the quasi-chronic infection equilibrium of the stochastic system. In addition, for completeness, we also obtain sufficient criteria for elimination of all infected CD4+ T cells and free virus particles. Finally, several examples together with comprehensive numerical simulations are conducted to support our analytic results.

Periodic Trajectories for HIV Dynamics in a Seasonal Environment With a General Incidence Rate

In this paper, we propose a five-dimensional nonlinear system of differential equations for the human immunodeficiency virus (HIV) including the B-cell functions with a general nonlinear incidence rate. The compartment of infected cells was subdivided into three classes representing the latently infected cells, the short-lived productively infected cells, and the long-lived productively infected cells. The basic reproduction number was established, and the local and global stability of the equilibria of the model were studied. A sensitivity analysis with respect to the model parameters was undertaken. Finally, some numerical simulations are presented to illustrate the theoretical findings.

Spatiotemporally Comparative Analysis of HIV, Pulmonary Tuberculosis, HIV-Pulmonary Tuberculosis Coinfection in Jiangsu Province, China.

Pulmonary tuberculosis (PTB) is a severe chronic communicable disease that causes a heavy disease burden in China. Human Immunodeficiency Virus (HIV) and PTB coinfection dramatically increases the risk of death. This study analyzes the spatiotemporal dynamics of HIV, PTB and HIV-PTB coinfection in Jiangsu Province, China, and explores the impact of socioeconomic determinants. The data on all notified HIV, PTB and HIV-PTB coinfection cases were extracted from Jiangsu Provincial Center for Disease Control and Prevention. We applied the seasonal index to identify high-risk periods of the disease. Time trend, spatial autocorrelation and SaTScan were used to analyze temporal trends, hotspots and spatiotemporal clusters of diseases. The Bayesian space-time model was conducted to examine the socioeconomic determinants. The case notification rate (CNR) of PTB decreased from 2011 to 2019 in Jiangsu Province, but the CNR of HIV and HIV-PTB coinfection had an upward trend. The seasonal index of PTB was the highest in March, and its hotspots were mainly distributed in the central and northern parts, such as Xuzhou, Suqian, Lianyungang and Taizhou. HIV had the highest seasonal index in July and HIV-PTB coinfection had the highest seasonal index in June, with their hotspots mainly distributed in southern Jiangsu, involving Nanjing, Suzhou, Wuxi and Changzhou. The Bayesian space-time interaction model showed that socioeconomic factor and population density were negatively correlated with the CNR of PTB, and positively associated with the CNR of HIV and HIV-PTB coinfection. The spatial heterogeneity andspatiotemporal clusters of PTB, HIV and HIV-PTB coinfection are exhibited obviously in Jiangsu. More comprehensive interventions should be applied to target TB in the northern part. While in southern Jiangsu, where the economic level is well-developed and the population density is high, we should strengthen the prevention and control of HIV and HIV-PTB coinfection.

HIV Dynamics with a Trilinear Antibody Growth Function and Saturated Infection Rate

The objective of this paper is to study a new mathematical model describing the human immunodeficiency virus (HIV). The model incorporates the impacts of cytotoxic T lymphocyte (CTL) immunity and antibodies with trilinear growth functions. The boundedness and positivity of solutions for non-negative initial data are proved, which is consistent with biological studies. The local stability of the equilibrium is established. Finally, numerical simulations are presented to support our theoretical findings.

Risk perception and vulnerabilities for HIV/AIDS among transgender women in Brazil: mixed methods approach

ABSTRACT Transgender women (TW) are a key population in the dynamics of human immunodeficiency virus (HIV) dissemination, although little is known about their perceptions of HIV risk. In this embedded, nested, mixed-methods study, we assessed factors associated with condomless sexual intercourse among TW and explored their risk perceptions and vulnerabilities regarding HIV exposure. The first phase involved a cross-sectional study, followed by qualitative interviews. Condomless sexual intercourse during their last sexual encounter was reported by 37.3% of participants, and 16.1% previously tested positive for HIV. Age older than 21 years, single status, and being a sex worker were protective factors for condomless intercourse. Otherwise, TW who reported a past sexual partner with a known sexually transmitted infection and those aware of post-exposure prophylaxis had a greater risk of condomless sexual intercourse (p < 0.05) during their most recent encounter. The qualitative interviews revealed that, despite TW being aware of their risk of contracting HIV, their vulnerabilities overlapped their risk perception, making them trivialize or ignore the risk. This study will help to understand the HIV dynamics among TW and contribute to further health research, education, policymaking, and planning associated with specific health strategies to promote the sexual health of TW.

Dynamical Behaviour and Chaotic Phenomena of HIV Infection through Fractional Calculus

The infection of human immunodeficiency virus (HIV) is a serious and potentially incurable infection. There is no cure for HIV and is a public health issue around the world. That is why, it is valuable to investigate the intricate phenomena of HIV infection and provide some control interventions to lessen its economic burden. In this research work, the dynamics of HIV via fractional calculus to conceptualize the intricate phenomena of this viral infection has been formulated and conceptualized. We have shown the rudimentary concept of fractional calculus in Atangana–Baleanu framework. A novel numerical technique is presented for the chaotic and dynamic behaviour of the proposed model. The oscillatory and chaotic phenomena of the system have been shown with the fluctuation of different input factors of the system. Furthermore, we have shown the affect of fractional order on the proposed system of HIV infection. Most critical input parameters are highlighted through numerical simulations and suggested control intervention to the policy makers. Finally, we have shown the stability result and the convergence condition for the proposed numerical scheme.

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;

Modeling the Effect of Reactive Oxygen Species and CTL Immune Response on HIV Dynamics

Individuals infected by human immunodeficiency virus (HIV) are under oxidative stress due to the imbalance between reactive oxygen species (ROS) production and elimination. This paper presents a mathematical model with the cytotoxic T lymphocytes (CTL) immune response to examine the role of ROS in the dynamics of HIV infection. We classify the equilibria of the model and study the stability of these equilibria. Numerical simulations show that incorporating ROS and CTL immune response into the model leads to very rich dynamics, including bistable phenomena and periodic solutions. Although the current antiretroviral therapy can suppress viral load to the undetectable level, it cannot eradicate the virus. A high level of ROS may be a factor for HIV persistence in patients despite suppressive therapy. These results suggest that oxidative damage and anti-oxidant therapy should be considered in the study of HIV infection and treatment.

Modeling and analysis of a within-host HIV/HTLV-I co-infection.

Human immunodeficiency virus (HIV) and human T-lymphotropic virus type I (HTLV-I) are two retroviruses that attack the {text {CD4}}^{+}T cells and impair their functions. Both HIV and HTLV-I can be transmitted between individuals through direct contact with certain body fluids from infected individuals. Therefore, a person can be co-infected with both viruses. HIV causes acquired immunodeficiency syndrome (AIDS), while HTLV-I is the causative agent for adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Several mathematical models have been developed in the literature to describe the within-host dynamics of HIV and HTLV-I mono-infections. However, modeling a within-host dynamics of HIV/HTLV-I co-infection has not been involved. The present paper is concerned with the formulation and investigation of 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 {text {CD4}}^{+}T cells, silent HIV-infected cells, active HIV-infected cells, silent HTLV-infected cells, Tax-expressing HTLV-infected cells, free HIV particles, HIV-specific CTLs and HTLV-specific CTLs. The HIV can spread by virus-to-cell transmission. On the other side, HTLV-I has two modes of transmission, (i) horizontal transmission via direct cell-to-cell contact through the virological synapse, and (ii) vertical transmission through the mitotic division of Tax-expressing HTLV-infected cells. The well-posedness of the model is established by showing that the solutions of the model are nonnegative and bounded. We define a set of 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 Lyapunov–LaSalle asymptotic stability theorem. 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.

Fractional Dynamics of HIV with Source Term for the Supply of New CD4+ T-Cells Depending on the Viral Load via Caputo–Fabrizio Derivative

Human immunodeficiency virus (HIV) is a life life-threatening and serious infection caused by a virus that attacks T-cells, which fight against infections and make a person susceptible to other diseases. It is a global public health problem with no cure; therefore, it is highly important to study and understand the intricate phenomena of HIV. In this article, we focus on the numerical study of the path-tracking damped oscillatory behavior of a model for the HIV infection of T-cells. We formulate fractional dynamics of HIV with a source term for the supply of new CD4+ T-cells depending on the viral load via the Caputo–Fabrizio derivative. In the formulation of fractional HIV dynamics, we replaced the constant source term for the supply of new T-cells from the thymus with a variable source term depending on the concentration of the viral load, and introduced a term that describes the incidence of the HIV infection of T-cells. We present a novel numerical scheme for fractional view analysis of the proposed model to highlight the solution pathway of HIV. We inspect the periodic and chaotic behavior of HIV for the given values of input factors using numerical simulations.