59
views
0
recommends
+1 Recommend
2 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Impact of COVID-19 on HIV Treatment and Research: A Call to Action

      review-article

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The impact of the COVID-19 pandemic is far reaching, with devastating effects on individuals, communities, and societies across the world. People with chronic health conditions may be at greater risk of contracting or experiencing complications from COVID-19. In addition to illness or death for those who contract the virus, the physical distancing required to flatten the curve of new cases is having a negative impact on the economy, the effects of which intersect with mental health and other existing health concerns, thus affecting marginalized communities. Given that HIV also has a disproportionate impact on marginalized communities, COVID-19 is affecting people with HIV (PWH) in unique ways and will continue to have an impact on HIV research and treatment after the COVID-19 crisis passes. Using the biopsychosocial framework to contextualize the impact of COVID-19 on PWH, the purpose of this review article is to: (1) outline the similarities and differences between the COVID-19 and HIV pandemics; (2) describe the current and future impact of COVID-19 on PWH; and (3) outline a call to action for scientists and practitioners to respond to the impact of COVID-19 on HIV prevention and treatment.

          Related collections

          Most cited references76

          • Record: found
          • Abstract: found
          • Article: not found

          Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

          Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p<0·0001), and d-dimer greater than 1 μg/mL (18·42, 2·64–128·55; p=0·0033) on admission. Median duration of viral shedding was 20·0 days (IQR 17·0–24·0) in survivors, but SARS-CoV-2 was detectable until death in non-survivors. The longest observed duration of viral shedding in survivors was 37 days. Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.
            • Record: found
            • Abstract: found
            • Article: not found

            Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1

            To the Editor: A novel human coronavirus that is now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (formerly called HCoV-19) emerged in Wuhan, China, in late 2019 and is now causing a pandemic. 1 We analyzed the aerosol and surface stability of SARS-CoV-2 and compared it with SARS-CoV-1, the most closely related human coronavirus. 2 We evaluated the stability of SARS-CoV-2 and SARS-CoV-1 in aerosols and on various surfaces and estimated their decay rates using a Bayesian regression model (see the Methods section in the Supplementary Appendix, available with the full text of this letter at NEJM.org). SARS-CoV-2 nCoV-WA1-2020 (MN985325.1) and SARS-CoV-1 Tor2 (AY274119.3) were the strains used. Aerosols (<5 μm) containing SARS-CoV-2 (105.25 50% tissue-culture infectious dose [TCID50] per milliliter) or SARS-CoV-1 (106.75-7.00 TCID50 per milliliter) were generated with the use of a three-jet Collison nebulizer and fed into a Goldberg drum to create an aerosolized environment. The inoculum resulted in cycle-threshold values between 20 and 22, similar to those observed in samples obtained from the upper and lower respiratory tract in humans. Our data consisted of 10 experimental conditions involving two viruses (SARS-CoV-2 and SARS-CoV-1) in five environmental conditions (aerosols, plastic, stainless steel, copper, and cardboard). All experimental measurements are reported as means across three replicates. SARS-CoV-2 remained viable in aerosols throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air. This reduction was similar to that observed with SARS-CoV-1, from 104.3 to 103.5 TCID50 per milliliter (Figure 1A). SARS-CoV-2 was more stable on plastic and stainless steel than on copper and cardboard, and viable virus was detected up to 72 hours after application to these surfaces (Figure 1A), although the virus titer was greatly reduced (from 103.7 to 100.6 TCID50 per milliliter of medium after 72 hours on plastic and from 103.7 to 100.6 TCID50 per milliliter after 48 hours on stainless steel). The stability kinetics of SARS-CoV-1 were similar (from 103.4 to 100.7 TCID50 per milliliter after 72 hours on plastic and from 103.6 to 100.6 TCID50 per milliliter after 48 hours on stainless steel). On copper, no viable SARS-CoV-2 was measured after 4 hours and no viable SARS-CoV-1 was measured after 8 hours. On cardboard, no viable SARS-CoV-2 was measured after 24 hours and no viable SARS-CoV-1 was measured after 8 hours (Figure 1A). Both viruses had an exponential decay in virus titer across all experimental conditions, as indicated by a linear decrease in the log10TCID50 per liter of air or milliliter of medium over time (Figure 1B). The half-lives of SARS-CoV-2 and SARS-CoV-1 were similar in aerosols, with median estimates of approximately 1.1 to 1.2 hours and 95% credible intervals of 0.64 to 2.64 for SARS-CoV-2 and 0.78 to 2.43 for SARS-CoV-1 (Figure 1C, and Table S1 in the Supplementary Appendix). The half-lives of the two viruses were also similar on copper. On cardboard, the half-life of SARS-CoV-2 was longer than that of SARS-CoV-1. The longest viability of both viruses was on stainless steel and plastic; the estimated median half-life of SARS-CoV-2 was approximately 5.6 hours on stainless steel and 6.8 hours on plastic (Figure 1C). Estimated differences in the half-lives of the two viruses were small except for those on cardboard (Figure 1C). Individual replicate data were noticeably “noisier” (i.e., there was more variation in the experiment, resulting in a larger standard error) for cardboard than for other surfaces (Fig. S1 through S5), so we advise caution in interpreting this result. We found that the stability of SARS-CoV-2 was similar to that of SARS-CoV-1 under the experimental circumstances tested. This indicates that differences in the epidemiologic characteristics of these viruses probably arise from other factors, including high viral loads in the upper respiratory tract and the potential for persons infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic. 3,4 Our results indicate that aerosol and fomite transmission of SARS-CoV-2 is plausible, since the virus can remain viable and infectious in aerosols for hours and on surfaces up to days (depending on the inoculum shed). These findings echo those with SARS-CoV-1, in which these forms of transmission were associated with nosocomial spread and super-spreading events, 5 and they provide information for pandemic mitigation efforts.
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              The reproductive number of COVID-19 is higher compared to SARS coronavirus

              Introduction In Wuhan, China, a novel and alarmingly contagious primary atypical (viral) pneumonia broke out in December 2019. It has since been identified as a zoonotic coronavirus, similar to SARS coronavirus and MERS coronavirus and named COVID-19. As of 8 February 2020, 33 738 confirmed cases and 811 deaths have been reported in China. Here we review the basic reproduction number (R 0) of the COVID-19 virus. R 0 is an indication of the transmissibility of a virus, representing the average number of new infections generated by an infectious person in a totally naïve population. For R 0 > 1, the number infected is likely to increase, and for R 0 < 1, transmission is likely to die out. The basic reproduction number is a central concept in infectious disease epidemiology, indicating the risk of an infectious agent with respect to epidemic spread. Methods and Results PubMed, bioRxiv and Google Scholar were accessed to search for eligible studies. The term ‘coronavirus & basic reproduction number’ was used. The time period covered was from 1 January 2020 to 7 February 2020. For this time period, we identified 12 studies which estimated the basic reproductive number for COVID-19 from China and overseas. Table 1 shows that the estimates ranged from 1.4 to 6.49, with a mean of 3.28, a median of 2.79 and interquartile range (IQR) of 1.16. Table 1 Published estimates of R 0 for 2019-nCoV Study (study year) Location Study date Methods Approaches R 0 estimates (average) 95% CI Joseph et al. 1 Wuhan 31 December 2019–28 January 2020 Stochastic Markov Chain Monte Carlo methods (MCMC) MCMC methods with Gibbs sampling and non-informative flat prior, using posterior distribution 2.68 2.47–2.86 Shen et al. 2 Hubei province 12–22 January 2020 Mathematical model, dynamic compartmental model with population divided into five compartments: susceptible individuals, asymptomatic individuals during the incubation period, infectious individuals with symptoms, isolated individuals with treatment and recovered individuals R 0 = \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$\beta$\end{document} / \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$\alpha$\end{document} \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$\beta$\end{document} = mean person-to-person transmission rate/day in the absence of control interventions, using nonlinear least squares method to get its point estimate \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{upgreek} \usepackage{mathrsfs} \setlength{\oddsidemargin}{-69pt} \begin{document} }{}$\alpha$\end{document} = isolation rate = 6 6.49 6.31–6.66 Liu et al. 3 China and overseas 23 January 2020 Statistical exponential Growth, using SARS generation time = 8.4 days, SD = 3.8 days Applies Poisson regression to fit the exponential growth rateR 0 = 1/M(−𝑟)M = moment generating function of the generation time distributionr = fitted exponential growth rate 2.90 2.32–3.63 Liu et al. 3 China and overseas 23 January 2020 Statistical maximum likelihood estimation, using SARS generation time = 8.4 days, SD = 3.8 days Maximize log-likelihood to estimate R 0 by using surveillance data during a disease epidemic, and assuming the secondary case is Poisson distribution with expected value R 0 2.92 2.28–3.67 Read et al. 4 China 1–22 January 2020 Mathematical transmission model assuming latent period = 4 days and near to the incubation period Assumes daily time increments with Poisson-distribution and apply a deterministic SEIR metapopulation transmission model, transmission rate = 1.94, infectious period =1.61 days 3.11 2.39–4.13 Majumder et al. 5 Wuhan 8 December 2019 and 26 January 2020 Mathematical Incidence Decay and Exponential Adjustment (IDEA) model Adopted mean serial interval lengths from SARS and MERS ranging from 6 to 10 days to fit the IDEA model, 2.0–3.1 (2.55) / WHO China 18 January 2020 / / 1.4–2.5 (1.95) / Cao et al. 6 China 23 January 2020 Mathematical model including compartments Susceptible-Exposed-Infectious-Recovered-Death-Cumulative (SEIRDC) R = K 2 (L × D) + K(L + D) + 1L = average latent period = 7,D = average latent infectious period = 9,K = logarithmic growth rate of the case counts 4.08 / Zhao et al. 7 China 10–24 January 2020 Statistical exponential growth model method adopting serial interval from SARS (mean = 8.4 days, SD = 3.8 days) and MERS (mean = 7.6 days, SD = 3.4 days) Corresponding to 8-fold increase in the reporting rateR 0 = 1/M(−𝑟)𝑟 =intrinsic growth rateM = moment generating function 2.24 1.96–2.55 Zhao et al. 7 China 10–24 January 2020 Statistical exponential growth model method adopting serial interval from SARS (mean = 8.4 days, SD = 3.8 days) and MERS (mean = 7.6 days, SD = 3.4 days) Corresponding to 2-fold increase in the reporting rateR 0 = 1/M(−𝑟)𝑟 =intrinsic growth rateM = moment generating function 3.58 2.89–4.39 Imai (2020) 8 Wuhan January 18, 2020 Mathematical model, computational modelling of potential epidemic trajectories Assume SARS-like levels of case-to-case variability in the numbers of secondary cases and a SARS-like generation time with 8.4 days, and set number of cases caused by zoonotic exposure and assumed total number of cases to estimate R 0 values for best-case, median and worst-case 1.5–3.5 (2.5) / Julien and Althaus 9 China and overseas 18 January 2020 Stochastic simulations of early outbreak trajectories Stochastic simulations of early outbreak trajectories were performed that are consistent with the epidemiological findings to date 2.2 Tang et al. 10 China 22 January 2020 Mathematical SEIR-type epidemiological model incorporates appropriate compartments corresponding to interventions Method-based method and Likelihood-based method 6.47 5.71–7.23 Qun Li et al. 11 China 22 January 2020 Statistical exponential growth model Mean incubation period = 5.2 days, mean serial interval = 7.5 days 2.2 1.4–3.9 Averaged 3.28 CI, Confidence interval. Figure 1 Timeline of the R 0 estimates for the 2019-nCoV virus in China The first studies initially reported estimates of R 0 with lower values. Estimations subsequently increased and then again returned in the most recent estimates to the levels initially reported (Figure 1). A closer look reveals that the estimation method used played a role. The two studies using stochastic methods to estimate R 0, reported a range of 2.2–2.68 with an average of 2.44. 1 , 9 The six studies using mathematical methods to estimate R 0 produced a range from 1.5 to 6.49, with an average of 4.2. 2 , 4–6 , 8 , 10 The three studies using statistical methods such as exponential growth estimated an R 0 ranging from 2.2 to 3.58, with an average of 2.67. 3 , 7 , 11 Discussion Our review found the average R 0 to be 3.28 and median to be 2.79, which exceed WHO estimates from 1.4 to 2.5. The studies using stochastic and statistical methods for deriving R 0 provide estimates that are reasonably comparable. However, the studies using mathematical methods produce estimates that are, on average, higher. Some of the mathematically derived estimates fall within the range produced the statistical and stochastic estimates. It is important to further assess the reason for the higher R 0 values estimated by some the mathematical studies. For example, modelling assumptions may have played a role. In more recent studies, R 0 seems to have stabilized at around 2–3. R 0 estimations produced at later stages can be expected to be more reliable, as they build upon more case data and include the effect of awareness and intervention. It is worthy to note that the WHO point estimates are consistently below all published estimates, although the higher end of the WHO range includes the lower end of the estimates reviewed here. R 0 estimates for SARS have been reported to range between 2 and 5, which is within the range of the mean R 0 for COVID-19 found in this review. Due to similarities of both pathogen and region of exposure, this is expected. On the other hand, despite the heightened public awareness and impressively strong interventional response, the COVID-19 is already more widespread than SARS, indicating it may be more transmissible. Conclusions This review found that the estimated mean R 0 for COVID-19 is around 3.28, with a median of 2.79 and IQR of 1.16, which is considerably higher than the WHO estimate at 1.95. These estimates of R 0 depend on the estimation method used as well as the validity of the underlying assumptions. Due to insufficient data and short onset time, current estimates of R 0 for COVID-19 are possibly biased. However, as more data are accumulated, estimation error can be expected to decrease and a clearer picture should form. Based on these considerations, R 0 for COVID-19 is expected to be around 2–3, which is broadly consistent with the WHO estimate. Author contributions J.R. and A.W.S. had the idea, and Y.L. did the literature search and created the table and figure. Y.L. and A.W.S. wrote the first draft; A.A.G. drafted the final manuscript. All authors contributed to the final manuscript. Conflict of interest None declared.

                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                24 June 2020
                June 2020
                : 17
                : 12
                : 4548
                Affiliations
                [1 ]Department of Psychology, University of South Florida St. Petersburg, 140 7th Avenue South, St. Petersburg, FL 33701, USA; kgabbido@ 123456usf.edu
                [2 ]Department of Psychological and Social Foundations, University of South Florida, 4202 E. Fowler Avenue, Tampa, FL 33620, USA; yaa1@ 123456usf.edu (P.H.); cholyfield@ 123456usf.edu (C.H.)
                Author notes
                [* ]Correspondence: chennevi@ 123456usf.edu
                Author information
                https://orcid.org/0000-0001-9900-4308
                Article
                ijerph-17-04548
                10.3390/ijerph17124548
                7345635
                32599783
                0416a7a9-956c-4c82-930c-450a96dcf987
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 27 May 2020
                : 14 June 2020
                Categories
                Review

                Public health
                covid-19,coronavirus,hiv,aids,health disparities
                Public health
                covid-19, coronavirus, hiv, aids, health disparities

                Comments

                Comment on this article

                Related Documents Log