Mycobacterium tuberculosis co-infection is associated with increased surrogate marker of the HIV reservoir

Xun, Jingna; Qi, Tangkai; Zou, Lei; Tang, Qi; Shen, Yinzhong; Yang, Junyang; Xie, Luman; Ji, Yongjia; Zhang, Renfang; Liu, Li; Wang, Jiangrong; Steinhart, Corklin R.; Wang, Zhenyan; Tang, Yang; Song, Wei; Sun, Jianjun; Cheng, Juan; Le, Xiaoqin; Wu, Huanmei; He, Xiaoqing; Chen, Rong; Lu, Hongzhou

doi:10.1186/s12981-020-00320-0

Cited by 11 publications

(11 citation statements)

References 29 publications

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“…Both longitudinal and cross-sectional studies, however, have shown that Mtb disease increases HIV-1 replication. 37 , 38 Increased rounds of virus replication generate a larger number of genetic variants. Thus, Mtb disease may augment humoral responses by increasing the diversity of the HIV-1 Env antigen encountered by antibody-producing cells.…”

Section: Resultsmentioning

confidence: 99%

Mycobacterium tuberculosis disease associates with higher HIV-1-specific antibody responses

Adeoye¹,

Nakiyingi²,

Moreau³

et al. 2023

iScience

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Section: Resultsmentioning

confidence: 99%

Mycobacterium tuberculosis disease associates with higher HIV-1-specific antibody responses

Adeoye¹,

Nakiyingi²,

Moreau³

et al. 2023

iScience

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“…Our previous multi-variable linear regression analysis showed that these factors did not independently associate with neutralization BP score after accounting for Mtb disease status (Table 1). Both longitudinal and cross-sectional studies have shown that Mtb disease increases HIV-1 replication (44, 45). Increased rounds of virus replication generate a larger number of genetic variants.…”

Section: Resultsmentioning

confidence: 99%

Mycobacterium tuberculosisdisease associates with higher HIV-1-specific antibody responses

Adeoye

Nakiyingi

Moreau

et al. 2022

Preprint

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Mycobacterium tuberculosis (Mtb) can enhance immune responses against unrelated pathogens. Although Mtb is the most common co-infection in people living with HIV (PWH), there has been no examination of its impact on HIV-1 immune responses. Plasma neutralization and antibody dependent cellular cytotoxicity (ADCC) was compared among PWH and Mtb disease (PWH/Active Mtb) and PWH/No Mtb both prior to and after antiretroviral treatment (ART) and completion of Mtb therapy. We assessed HIV-1 sequences, total antibody quantities and isotypes, and plasma cytokine levels to ascertain mechanisms that affect humoral responses. HIV-1 neutralizing antibodies (nAbs) were broader and more potent in PWH/Active Mtb as compared to PWH/No Mtb, and nAbs increased among PWH who developed Mtb after ART initiation. ADCC was also higher in the PWH who had Mtb disease after starting ART. PWH/Active Mtb as compared to PWH/No Mtb had unique HIV-1 envelope sequence motifs associated with neutralization resistance further implying differences in humoral selection. The Mtb-linked antibody augmentation associated with elevated plasma cytokine levels important for B cells and antibody production, namely interleukin-6, a proliferation-inducing ligand (APRIL), and B-cell activating factor (BAFF). Increased plasma virus levels, greater HIV-1 envelope diversity, higher levels of all antibodies, and cross-reactive responses did not explain the enhanced HIV-1 humoral responses in those with Mtb. Mtb disease enhances HIV-1 humoral responses likely by perturbing pathways important for antibody production in lymphoid tissue that has both pathogens. These findings have implications for using antibody-based therapies and inducing optimal HIV-1 antibody responses.

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“…The effects of SARS-CoV-2 on the lung HIV reservoir remain largely unknown. It is plausible that SARS-CoV-2-induced immune activation, similarly to what has been reported in PLWH with tuberculosis and other pulmonary infections, could stimulate viral replication and clonal expansion of HIV-infected cells but no studies have yet been published to support or refute this hypothesis (229,256).…”

Section: Hiv and Sars-cov-2 Infectionmentioning

confidence: 99%

Pulmonary Immune Dysregulation and Viral Persistence During HIV Infection

2022

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Despite the success of antiretroviral therapy (ART), people living with HIV continue to suffer from high burdens of respiratory infections, lung cancers and chronic lung disease at a higher rate than the general population. The lung mucosa, a previously neglected HIV reservoir site, is of particular importance in this phenomenon. Because ART does not eliminate the virus, residual levels of HIV that remain in deep tissues lead to chronic immune activation and pulmonary inflammatory pathologies. In turn, continuous pulmonary and systemic inflammation cause immune cell exhaustion and pulmonary immune dysregulation, creating a pro-inflammatory environment ideal for HIV reservoir persistence. Moreover, smoking, gut and lung dysbiosis and co-infections further fuel the vicious cycle of residual viral replication which, in turn, contributes to inflammation and immune cell proliferation, further maintaining the HIV reservoir. Herein, we discuss the recent evidence supporting the notion that the lungs serve as an HIV viral reservoir. We will explore how smoking, changes in the microbiome, and common co-infections seen in PLWH contribute to HIV persistence, pulmonary immune dysregulation, and high rates of infectious and non-infectious lung disease among these individuals.

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Mycobacterium tuberculosis co-infection is associated with increased surrogate marker of the HIV reservoir

Cited by 11 publications

References 29 publications

Mycobacterium tuberculosis disease associates with higher HIV-1-specific antibody responses

Mycobacterium tuberculosis disease associates with higher HIV-1-specific antibody responses

Mycobacterium tuberculosisdisease associates with higher HIV-1-specific antibody responses

Pulmonary Immune Dysregulation and Viral Persistence During HIV Infection

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