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HIV-1 IMMUNITY

HIV-1-induced inflammation shapes innate immunity and induces adaptive traits in NK cells

Nature Immunology volume 21, pages 245–247 (2020)Cite this article

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Chronic inflammation associated with HIV-1 infection disrupts the homeostasis of gut-resident innate lymphoid cells and induces the generation and expansion of adaptive NK cells expressing TCF7, a transcription factor that sustains their effector functions and memory-like properties.

The introduction of antiretroviral therapy (ART) greatly improved the clinical outcome of HIV-1 infection by preventing its progression toward AIDS. Globally, 37.9 million people are living with HIV-1 infection, and more than 23 million people currently receive ART (https://www.who.int/gho/hiv/en/). The administration of ART early after infection ensures a faster and more efficient reconstitution of the immune system, limits the establishment of HIV-1 latency and reduces viral transmission to seronegative partners. However, the overall mortality rate of HIV-1 infection continues to increase, and the onset of severe and life-threatening chronic comorbidities associated with HIV-1 infection (that is, cardiovascular diseases, neurocognitive dysfunctions and cancer) still represent an unmet clinical need due to abnormal and dysfunctional immune activation that, in turn, leads to systemic chronic inflammation1. Indeed, pathologic high plasma levels of several inflammatory markers and cytokines, such as interleukin (IL)-6, soluble CD14 (sCD14) and C-reactive protein, accelerate disease progression and death in even those ART-treated HIV-1 infected patients with undetectable viremia and optimal CD4+ T cell recovery1. The pathophysiology of this persistent high inflammation is still controversial and is being debated in the era of modern ART. In this issue of Nature Immunology, Wang et al.2 shed new light on this matter, as ongoing but clinically undetectable HIV-1 replication does not alone explain the establishment of persistent high degrees of immune activation.

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Fig. 1: HIV-1-associated inflammation alters the homeostasis of gut-resident and circulating lymphocytes.

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Authors and Affiliations

  1. Unit of Clinical and Experimental Immunology, Humanitas Clinical and Research Center, Rozzano, Milan, Italy

    Joanna Mikulak, Clara Di Vito & Domenico Mavilio

  2. Department of Medical Biotechnologies and Translational Medicine (BioMeTra), University of Milan, Milan, Italy

    Joanna Mikulak, Clara Di Vito & Domenico Mavilio

Authors
  1. Joanna Mikulak
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  2. Clara Di Vito
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  3. Domenico Mavilio
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Correspondence to Domenico Mavilio.

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Mikulak, J., Di Vito, C. & Mavilio, D. HIV-1-induced inflammation shapes innate immunity and induces adaptive traits in NK cells. Nat Immunol 21, 245–247 (2020). https://doi.org/10.1038/s41590-020-0615-7

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