During global pandemics, such as coronavirus disease 2019 (COVID-19), crisis communication is indispensable in dispelling fears, uncertainty, and unifying individuals worldwide in a collective fight against health threats. Inadequate crisis communication can bring dire personal and economic consequences. Mounting research shows that seemingly endless newsfeeds related to COVID-19 infection and death rates could considerably increase the risk of mental health problems. Unfortunately, media reports that include infodemics regarding the influence of COVID-19 on mental health may be a source of the adverse psychological effects on individuals. Owing partially to insufficient crisis communication practices, media and news organizations across the globe have played minimal roles in battling COVID-19 infodemics. Common refrains include raging QAnon conspiracies, a false and misleading “Chinese virus” narrative, and the use of disinfectants to “cure” COVID-19. With the potential to deteriorate mental health, infodemics fueled by a kaleidoscopic range of misinformation can be dangerous. Unfortunately, there is a shortage of research on how to improve crisis communication across media and news organization channels. This paper identifies ways that legacy media reports on COVID-19 and how social media-based infodemics can result in mental health concerns. This paper discusses possible crisis communication solutions that media and news organizations can adopt to mitigate the negative influences of COVID-19 related news on mental health. Emphasizing the need for global media entities to forge a fact-based, person-centered, and collaborative response to COVID-19 reporting, this paper encourages media resources to focus on the core issue of how to slow or stop COVID-19 transmission effectively.

High-throughput sequencing platforms provide an approach for detecting rare HIV-1 variants and documenting more fully quasispecies diversity. We applied this technology to the V3 loop-coding region of env in samples collected from 4 chronically HIV-infected subjects in whom CCR5 antagonist (vicriviroc [VVC]) therapy failed. Between 25,000–140,000 amplified sequences were obtained per sample. Profound baseline V3 loop sequence heterogeneity existed; predicted CXCR4-using populations were identified in a largely CCR5-using population. The V3 loop forms associated with subsequent virologic failure, either through CXCR4 use or the emergence of high-level VVC resistance, were present as minor variants at 0.8–2.8% of baseline samples. Extreme, rapid shifts in population frequencies toward these forms occurred, and deep sequencing provided a detailed view of the rapid evolutionary impact of VVC selection. Greater V3 diversity was observed post-selection. This previously unreported degree of V3 loop sequence diversity has implications for viral pathogenesis, vaccine design, and the optimal use of HIV-1 CCR5 antagonists.

In HIV-1-infected, treatment-experienced patients, vicriviroc demonstrated potent virologic suppression through 24 weeks. The relationship of vicriviroc to malignancy is uncertain. Further development of vicriviroc in treatment-experienced patients is warranted.

Little is known about the in vivo development of resistance to human immunodeficiency virus type 1 (HIV-1) CCR5 antagonists. We studied 29 subjects with virologic failure from a phase IIb study of the CCR5 antagonist vicriviroc (VCV) and identified one individual with HIV-1 subtype C who developed VCV resistance. Studies with chimeric envelopes demonstrated that changes within the V3 loop were sufficient to confer VCV resistance. Resistant virus showed VCV-enhanced replication, cross-resistance to another CCR5 antagonist, TAK779, and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004. Pretreatment V3 loop sequences reemerged following VCV discontinuation, implying that VCV resistance has associated fitness costs.The human immunodeficiency virus type 1 (HIV-1) envelope third variable loop (V3) is the major structural element of gp120 that determines coreceptor recognition and specificity (9,15,16). Vicriviroc (VCV; Schering-Plough) and maraviroc (Selzentry; Pfizer) are allosteric noncompetitive antagonists that bind to similar sites on CCR5 and antagonize the gp120-CCR5 interaction (19). To date, data on resistance to these agents have come largely from in vitro selection studies. Phenotypically, resistance manifests as a plateau in the maximum achievable suppression of viral replication (19). This plateau, referred to as the percent maximal inhibition, correlates with viral adaptation to the use of the inhibitor-bound form of CCR5 for entry (13,21). Genotypically, VCV resistance has been associated with a variety of amino-acid-changing mutations throughout the envelope gene (env) that most often involve V3 but whose effect on drug susceptibility depends on the env backbone into which they are introduced (5). In vitro data suggest that resistance to the closely related CCR5 antagonist AD101 does not confer a significant loss of viral fitness (1, 8). In vivo resistance to the CCR5 antagonists remains poorly defined.To study the emergence of VCV resistance in vivo, we monitored subjects enrolled in ACTG 5211, a 48-week study of VCV in 118 HIV-1-infected, treatment-experienced subjects (3). Among the 90 subjects receiving VCV, we studied all 29 who experienced protocol-defined virologic failure. We amplified full-length HIV-1 env from plasma samples collected during the period from study entry through week 48. These env sequences were used to generate pseudovirions for examining VCV susceptibility and coreceptor usage in the PhenoSense entry susceptibility and Trofile assays (Monogram Biosciences), respectively (20,22). In 28 of 29 subjects analyzed, no evidence of decreased VCV susceptibility was observed (data not shown). Samples from the remaining subject demonstrated increasing VCV resistance over 28 weeks (Fig. 1). This subject, randomly assigned to receive 10 mg of VCV daily, experienced protocol-defined virologic failure at week 16 but continued VCV treatment through week 28 (see Fig. S1 in the supplemental material). Samples from 13 of the 29 subjects showed the emergence...