A community psychology for migrant justice: Critically examining border violence and resistance during the COVID‐19 syndemic

This article explores the magnifying lenses of the COVID‐19 syndemic to highlight how people racialized as migrants and refugees have been—and continue to be— disproportionally harmed. We use empirical evidence collected in our scholarly/activist work in Europe, Africa, South Asia, and the United States to examine migrant injustice as being produced by a combination of power structures and relations working to maintain colonial global orders and inequalities. This is what has been defined as “border imperialism.” Our data, complemented by evidence from transnational solidarity groups, show that border imperialism has further intersected with the hygienic‐sanitary logics of social control at play during the COVID‐19 period. This intersection has resulted in increasingly coercive methods of restraining people on the move, as well as in increased—and new—forms of degradation of their lives, that is, an overall multiplication of border violences. At the same time, however, COVID‐19 has provided a unique opportunity for grassroot solidarity initiatives and resistance led by people on the move to be amplified and extended. We conclude by emphasizing the need for community psychologists to take a more vigorous stance against oppressive border imperialist regimes and the related forms of violence they re/enact. </p

Putative binding mode of RMC6 and critical residues individuated for RMNC6 binding in the pocket 1.

<p>(A) binding mode; (B) 2D depiction of RMNC6 and its respective interactions with RT residues: pale yellow sphere indicates hydrophobic interactions with lipophilic residues. Red arrow indicates an hydrogen bond (HB) acceptor interaction, green HB donor, while the violet sphere represents the aromatic π-π stacking interaction.</p

¹H NMR spectra of MeOH/H₂O extract of <i>H</i>. <i>scruglii</i>.

<p>Numbers indicate the diagnostic signals of the isolated secondary metabolites 1–6.</p

Chemical structure of the isatin derivative RMNC6.

<p>Chemical structure of the isatin derivative RMNC6.</p

Yonetani-Theorell plot of the combination of RMNC6 and EFV on the HIV-1 RT RNA- dependent DNA polymerase activity.

<p>HIV-1 RT was incubated in the presence of RMNC6 alone (●) or in presence of different concentrations of EFV: 4 nM (Δ), 8 nM (■) and 16 nM (☐).</p

Effect of RT inhibitors on the thermal stability of p66/p51 HIV-1 RT.

<p>(A). The melting temperature of HIV-1 RT was measured by differential scanning fluorimetry in the presence of increasing concentrations of different inhibitors: (▼) Efavirenz (EFV), (○) β-thujaplicinol (BTP), (Δ) 2-(3, 4-dihydroxyphenyl)-5, 6-dimethylthieno[2, 3-d]pyrimidin-4(3H)-one (VU) and (●) RMNC6. (B). Maximum HIV-1 RT thermal shift (ΔTm) observed in the presence of 50 μM concentration of compounds. ΔTm values are the average of triplicate analysis, standard deviations are indicated as bars.</p

Binding sites of RMNC6 individuated after blind docking experiments on the whole wt HIV-1 RT structure.

<p>Binding sites of RMNC6 individuated after blind docking experiments on the whole wt HIV-1 RT structure.</p

Chemical structures of known metabolites isolated from <i>H</i>. <i>scruglii</i>.

<p>Chemical structures of known metabolites isolated from <i>H</i>. <i>scruglii</i>.</p

Time-of-addition assay.

<p>The target of the antiviral compound <b>3</b> (Cp3) was identified by comparing its activity in the time scale to those of reference drugs: Maraviroc (MCV, entry inhibitor), Lamivudine (LAM, RT inhibitor), Dolutegravir (DTG, IN inhibitor). Cp3 was ineffective once the virus retrotranscribed its genome.</p

Antiviral activity of compounds 1, 2 and 3 on HIV AD8 laboratory strain in TZM-bl cells.

<p>Cells were infected with 300 TCID50/mL and treated with compounds isolated from <i>H</i>. <i>scruglii</i> at seven different concentration. EC₅₀ values ranged from 3.5 to 8 <b>μ</b>M. Only active compounds were shown.</p