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- Hamedi, Mahiar, et al.
(författare)
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Polypeptide-guided assembly of conducting polymer nanocomposites
- 2010
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Ingår i: NANOSCALE. - : Royal Society of Chemistry. - 2040-3364 .- 2040-3372. ; 2:10, s. 2058-2061
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Tidskriftsartikel (refereegranskat)abstract
- A strategy for fabrication of electroactive nanocomposites with nanoscale organization, based on self-assembly, is reported. Gold nanoparticles are assembled by a polypeptide folding-dependent bridging. The polypeptides are further utilized to recruit and associate with a water soluble conducting polymer. The polymer is homogenously incorporated into the nanocomposite, forming conducting pathways which make the composite material highly conducting.
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| 4. |
- Dahl, Göran, et al.
(författare)
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Resistance profiling of hepatitis C virus protease inhibitors using full-length NS3
- 2007
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Ingår i: Antiviral Therapy. - 1359-6535 .- 2040-2058. ; 12:5, s. 733-740
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Tidskriftsartikel (refereegranskat)abstract
- Background: The NS3 protease of hepatitis C virus (HCV) is a prime target for anti-HCV drugs but resistance towards inhibitors of the enzyme is likely to emerge because of mutations in the viral genome that modify the structure of the protein. Enzyme inhibition data supporting this is limited to studies with few compounds and analysis performed with truncated NS3. Experimental: The potential of HCV acquiring resistance towards NS3 protease inhibitors and the structural features associated with resistance has been explored with a series of inhibitors and by using full-length NS3 protease/helicase variants with amino acid substitutions (A156T, D168V and R155Q) in the protease domain. Results: The A156T and D168V substitutions did not influence the kinetic properties of the protease, whereas the R155Q substitution reduced the catalytic efficiency 20 times, as compared with the wild type. Inhibition studies revealed that these substitutions primarily affected the potency of compounds which effectively inhibit the wild-type enzyme, and had little effect on weak or moderate inhibitors. As a consequence, all compounds had similar inhibitory potencies to the substituted enzyme variants. An exception was VX-950, which inhibited the D168V enzyme more efficiently than the wild type. For this inhibitor, the present data correlated better with replicon data than data from assays with truncated enzyme. Conclusions: These results have provided a structural basis for designing inhibitors that may be less susceptible to resistance by three known mutations, and suggest that the present variants of full-length NS3 constitute effective models for resistance profiling of NS3 protease inhibitors.
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| 5. |
- Klingström, Jonas, et al.
(författare)
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Passive immunization protects cynomolgus macaques against Puumala hantavirus challenge.
- 2008
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Ingår i: Antiviral Therapy. - 1359-6535 .- 2040-2058. ; 13:1, s. 125-33
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Hantaviruses cause two severe and often fatal human diseases: haemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Presently, there is no effective prevention available for HFRS or HPS. Here, we studied the effect of passive immunization on the course of infection in cynomolgus macaques challenged with wild-type Puumala hantavirus (PUUV-wt). METHODS: A pool of serum drawn from previously PUUV-wt-infected monkeys was used for immunization; a pool of serum from the same monkeys that was obtained before infection was used as a control. Immunizations were administered 3 days before and 15 days after challenge with PUUV-wt. After challenge, monkeys were sampled once a week and analysed for PUUV-infection markers. RESULTS: All three monkeys treated with non-immune serum became positive for PUUV RNA in plasma and showed PUUV nucleocapsid-specific immunoglobin M (IgM) responses after challenge. In contrast, no PUUV RNA or anti-PUUV-specific IgM response was detected in the three passively immunized monkeys. As seen in PUUV-infected humans, the control monkeys showed a marked decrease in the amount of platelets and increased levels of creatinine, interleukin (1L)-6, IL-10, and tumour necrosis factor (TNF) after inoculation. In contrast, no marked changes in the amount of platelets were observed in the immunized monkeys and they did not show increased levels of creatinine, IL-6, IL-10 and TNF after virus challenge. CONCLUSION: The results show that passive immunization in monkeys, using serum from previously hantavirus-infected monkeys, can induce sterile protection and protect against pathogenesis. Convalescent-phase antibodies may represent a potential therapy that can induce immediate protection against HFRS and HPS.
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| 8. |
- Lyons, A, et al.
(författare)
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Outcomes of etravirine-based antiretroviral treatment in treatment-experienced children and adolescents living with HIV in Europe and Thailand
- 2022
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Ingår i: Antiviral therapy. - : SAGE Publications. - 2040-2058 .- 1359-6535. ; 27:3, s. 13596535221092182-
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Tidskriftsartikel (refereegranskat)abstract
- Etravirine (ETR) is approved as a component of second or third-line antiretroviral treatment (ART) for children living with HIV. We assessed the outcomes of ETR-based ART in children in routine care in Europe and Thailand. Methods Data on children aged <18 years at ETR start were pooled from 17 observational cohorts. Characteristics at ETR start, immunological and virological outcomes at 12 months, discontinuations, adverse events (AEs) and serious adverse events (SAEs) were described. Follow-up was censored at ETR discontinuation, death or last visit. Results 177 children ever received ETR. At ETR start, median [IQR] age was 15 [12,16] years, CD4 count 480 [287, 713] cells/mm3, 70% had exposure to ≥3 ART classes and 20% had viral load (VL) <50 copies/mL. 95% received ETR in combination with ≥1 potent drug class, mostly protease inhibitor-based regimens. Median time on ETR was 24 [7, 48] months. Amongst those on ETR at 12 months ( n=141), 69% had VL<50 copies/mL. Median CD4 increase since ETR start ( n=83) was 147 [16, 267] cells/mm3. Overall, 81 (46%) discontinued ETR by last follow-up. Median time to discontinuation was 23 [8, 47] months. Common reasons for discontinuation were treatment simplification (19%), treatment failure (16%) and toxicity (12%). Eight children (5%) had AEs causally associated with ETR, all dermatological/hypersensitivity reactions. Two were SAEs, both Stevens–Johnson Syndrome in children on regimens containing ETR and darunavir and were causally related to either drugs; both resolved following ART discontinuation. Conclusion Children receiving ETR were predominantly highly treatment-experienced, over two-thirds were virally suppressed at 12 months.
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