During chronic HIV infection, immune cells become increasingly dysfunctional and exhausted. Little is known about how immune functions are restored after initiation of antiretroviral therapy (ART). In this study, we assessed cellular and metabolic activity and evaluated the effect of individual antiretrovirals on cellular subsets ex vivo in ART-treated and treatment-naive chronically HIV-infected individuals. We observed that cellular respiration was significantly decreased in most immune cells in chronic HIV infection. The respiration was correlated to immune activation and the inhibitory receptor programmed cell death 1 on CD8 ⁺ T cells. ART restored the metabolic phenotype, but the respiratory impairment persisted in CD4 ⁺ T cells. This was particularly the case for individuals receiving integrase strand transfer inhibitors. CD4 ⁺ T cells from these individuals showed a significant reduction in ex vivo proliferative capacity compared with individuals treated with protease inhibitors or nonnucleoside reverse transcriptase inhibitors. We noticed a significant decrease in respiration of cells treated with dolutegravir (DLG) or elvitegravir (EVG) and a switch from polyfunctional to TNF-α–dominated “stress” immune response. There was no effect on glycolysis, consistent with impaired mitochondrial function. We detected increased levels of mitochondrial ROS and mitochondrial mass. These findings indicate that EVG and DLG use is associated with slow proliferation and impaired respiration with underlying mitochondrial dysfunction, resulting in overall decreased cellular function in CD4 ⁺ T cells.

Journal of Medical Internet Research - International Scientific Journal for Medical Research, Information and Communication on the Internet #Preprint #PeerReviewMe: Warning: This is a unreviewed preprint. Readers are warned that the document has not been peer-reviewed by expert/patient reviewers or an academic editor, may contain misleading claims, and is likely to undergo changes before final publication, if accepted, or may have been rejected/withdrawn. Readers with interest and expertise are encouraged to sign up as peer-reviewer, if the paper is within an open peer-review period. Please cite this preprint only for review purposes or for grant applications and CVs (if you are the author). A decreasing number of dermatologists and an increasing number of patients in Western countries have led to a relative lack of clinicians providing expert dermatologic care. This, in turn, has prolonged wait times for patients to be examined, putting them at risk. Store-and-forward teledermatology improves patient access to dermatologists through asynchronous consultations, reducing wait times to obtain a consultation. However, live video conferencing as a synchronous service is also frequently used by practitioners because it allows immediate interaction between patient and physician. This raises the question of which of the two approaches is superior in terms of quality of care and convenience. There are pros and cons for each in terms of technical requirements and features. This viewpoint compares the two techniques based on a literature review and a clinical perspective to help dermatologists assess the value of teledermatology and what techniques would be valuable in their practice.

HIV infection is a risk factor for the development of Herpes zoster (HZ) and its complications. Prior to antiretroviral therapy (ART), HZ incidence in HIV-infected individuals ranged from 2.9–5.1/100 person-years. There is limited evidence for the impact of ART on HZ occurrence among HIV-infected adults. We analysed the incidence of, and risk factors for, HZ in a large cohort of German HIV-positive patients.

Co-infections with HBV (hepatitis B virus) occur in HIV (human immunodeficiency virus) patients frequently. It has been reported that an effective treatment of HIV can also lead to a suppression of HBV and to anti-HBs seroconversion in HBV-infected patients. Here, we report a spontaneous reactivation of HBV replication in an HIV-infected patient with anti-HBc as the only marker of chronic HBV infection. The patient was known to be coinfected with HIV and HBV for years and the HBV DNA was measured repeatedly at low levels. A significant increase of HBV DNA up to 1.7x107 IU/ml was found accompanied with clinical symptoms of hepatitis. Multiple mutations occurred in the S gene during the flare-up of HBV as shown by sequencing, including I103T, K122R, M133I, F134V, D144E, V164E and L175S. Anti-HIV/HBV treatment led to a resolution of symptoms and to a decrease in the HIV RNA and HBV DNA viral load. It is possible that the accumulated mutations during HBV replication were selected and responsible for the reactivation.

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