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PEG IFN alpha-2a (CAP/CTM HCV 2.0)

✓ Approved

Roche · Companion diagnostic · Companion diagnostic

What is PEG IFN alpha-2a?

PEG IFN alpha-2a is a companion diagnostic developed by Roche. It is approved for therapeutic indications via others.

Drug Profile

Brand NamesCAP/CTM HCV 2.0
CompanyRoche
Drug ClassCompanion diagnostic
RouteOthers
StatusApproved
Sources: ClinicalTrials.gov, Roche

Related Research Articles

PubMedJournal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy2026-07-17

Mycoplasma Pneumonia Diagnostic Prediction Score: Is it possible to differentiate between Mycoplasma pneumoniae pneumonia and SARS-CoV-2 pneumonia?

Miyashita Naoyuki N, Nakamori Yasushi Y, Ogata Makoto M, Fukuda Naoki N et al.

The Mycoplasma Pneumonia Diagnostic Prediction Score, recommended in pneumonia guidelines, is a useful method for differentiating Mycoplasma pneumoniae pneumonia from bacterial pneumonia. On the other hand, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a common microorganism in community-acquired pneumonia, so we investigated whether the Mycoplasma Score can differentiate between M. pneumoniae pneumonia and SARS-CoV-2 pneumonia. Analysis was performed on 162 patients with M. pneumoniae, 422 patients with the Ancestral strain, 262 with the Alpha variant, 274 with the Delta variant, and 1,241 with the Omicron variant. When using the Mycoplasma Score, the sensitivity for predicting M. pneumoniae pneumonia was 71.8%. The diagnostic specificity was 81.3% for the Ancestral strain, 81.7% for the Alpha variant, 77.4% for the Delta variant, and 88.2% for the Omicron variant. The specificity for all SARS-CoV-2 pneumonia cases was 84.8%. When targeting the currently circulating Omicron variant, the diagnostic specificity ranged from 83.9% to 92.7%, showing differences among subvariants. Differences between the two groups were identified using four parameters: age, underlying disease, severity of cough, and use of rapid diagnostic methods. When comparing M. pneumoniae pneumonia and SARS-CoV-2 pneumonia, the diagnostic sensitivity of the Mycoplasma Pneumonia Diagnostic Prediction Score was 71.8%, and the diagnostic specificity was 84.8%. However, when targeting the currently circulating SARS-CoV-2 Omicron variant pneumonia, the diagnostic specificity increased to 88.2%, suggesting that it is possible to differentiate between M. pneumoniae pneumonia and SARS-CoV-2 pneumonia. However, the specificity is lower than that for differentiating bacterial pneumonia.

PMID 42463011
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PubMedParasitology international2026-07-17

Pyrethroid resistance intensity and mechanisms in Anopheles gambiae sensu lato (Diptera: Culicidae) from Oyo State, Nigeria.

Ibrahim Kolade T T, Braimah Jafar A A, Oyebamiji David A A, Obasi Nnennaya I I et al.

Pyrethroid resistance in Anopheles gambiae sensu lato (s.l.) is increasing across Nigeria and threatens the effectiveness of long-lasting insecticidal nets (LLINs) and other pyrethroid-based interventions across Nigeria. This study quantified resistance levels, intensity, and metabolic contributions in An. gambiae s.l. populations across ecologically distinct zones of Oyo State, southwestern Nigeria, to generate evidence for locally tailored vector control strategies. Between May and September 2018, immature stages of Anopheles gambiae sensu lato were collected from six Local Government Areas in Oyo State, Nigeria, with 10-15 larval habitats sampled per LGA using standard dipping procedures. Specimens were reared to adulthood under controlled insectary conditions (27 ± 2 °C; 75-84% Relative Humidity) before testing. For each insecticide in each LGA, approximately 450-550 non-blood-fed female mosquitoes were evaluated in accordance with WHO testing procedures. Susceptibility to alpha-cypermethrin (12.5 μg/bottle), deltamethrin (12.5 μg/bottle), and permethrin (21.5 μg/bottle) was determined using the CDC bottle bioassay at diagnostic concentrations (1×), with standard replicate batches per assay. Populations exhibiting resistance at 1× were further examined using elevated concentrations (2×, 5×, and 10×) to quantify resistance intensity. The involvement of metabolic detoxification was assessed through the contribution of cytochrome P450-mediated resistance mechanisms. A total of 9000 female mosquitoes were exposed to WHO diagnostic (1×) and elevated (2 × -10×) concentrations of alpha-cypermethrin, deltamethrin, and permethrin, complemented with piperonyl butoxide (PBO) synergist assays. At diagnostic dose, resistance was widespread, with mortality ranging from 5% (Egbeda) to 65% (Akinyele) for permethrin, 38.8-97% for alpha-cypermethrin, and 23-78% for deltamethrin, indicating significant spatial heterogeneity. Permethrin exhibited the highest resistance intensity, with incomplete mortality recovery even at 10×, while alpha-cypermethrin and deltamethrin showed full susceptibility restoration at 5× and 2×, respectively. Statistical analysis confirmed significant variation among LGAs (χ2, P < 0.001). Knockdown responses were reduced in Atiba, Afijio, and Egbeda, where several populations failed to reach 95% knockdown within 60 min. PBO pre-exposure fully restored susceptibility to alpha-cypermethrin (100%) across resistant LGAs, while deltamethrin showed partial recovery. In contrast, permethrin mortality remained incomplete (47-94%) after PBO, indicating limited metabolic involvement and likely target-site resistance. Overall, the findings demonstrate intense, spatially heterogeneous pyrethroid resistance driven by multiple mechanisms, with important implications for malaria vector control. While PBO-based LLINs may provide partial mitigation, they are unlikely to fully address the complexity of resistance observed across the study area. Consequently, sustained control in Oyo State will require complementary and alternative strategies, including next-generation dual-active-ingredient nets and other non-pyrethroid interventions.

PMID 42463059
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PubMedNature communications2026-07-17

Triple IFN pathway deficiency sensitizes mice to human respiratory virus infection independent of human viral receptor expression.

Fan Qinghong Q, Pan Meifang M, Jiang Mengling M, Feng Chengqian C et al.

Interferon (IFN) pathways form the innate barrier against viral invasion and partial deficiency in these pathways allows human virus infection. Whether a complete IFN pathway deficiency could confer the susceptibility to human viral infection independent of expressing the human viral receptor remains unknown. We develop an innate immunity severely deficient mouse model, designated AGL, which features one-step knock-out of the IFNAR, IFNGR and IFNLR. The AGL mice become susceptible to diverse representative human respiratory viruses, including adenovirus type 55 (HAdV-55; double-stranded DNA), human monkeypox virus (MPXV) clade IIb (double-stranded DNA), parainfluenza virus (PIV; negative-sense single-stranded RNA), and the clinically isolated SARS-CoV-2 delta variant (positive-sense single-stranded RNA). Our results suggest that the type III IFN pathway constitutes a backup layer of antiviral frontline beneath the type I and II IFN pathways. In addition, proof-of-concept studies testing MPXV and PIV antivirals highlight the translational value of AGL mice. The AGL mice, as a universal model, substantially enhance the ability to investigate both emerging and established viruses without the need for tailored mouse models.

PMID 42463654
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PubMedFrontiers in medicine2026-07-17

Identification of key vaginal microbial signatures and immune remodeling associated with HR-HPV clearance following Kushen Gel treatment: a longitudinal analysis.

Wang Ying Y, Pan Shuheng S, Zhang Fengying F, Ma Huimin H et al.

Persistent high-risk human papillomavirus (HR-HPV) infection drives cervical carcinogenesis, often exacerbated by vaginal dysbiosis and localized immune dysfunction. Kushen Gel shows clinical promise, yet its impact on microbial-immune crosstalk during HR-HPV clearance remains unclear. This study elucidates the microbial remodeling and immune shifts associated with Kushen Gel-mediated HR-HPV regression. A retrospective analysis of 230 vaginal swabs (130 pre-treatment, 100 post-treatment) via 16S rRNA sequencing characterized community structural shifts. Subsequently, a prospective cohort of 35 patients with persistent HR-HPV infection (defined as laboratory-confirmed positive HR-HPV DNA for ≥12 months) validated clinical outcomes (HR-HPV clearance, vaginal pH, Nugent scores) alongside paired 16S rRNA sequencing and ELISA-based quantification of cervicovaginal cytokines (IL-8, IL-6, TNF-α, IFN-γ). Kushen Gel intervention significantly decreased microbial alpha diversity and was associated with a distinct beta-diversity shift toward a stable, Lactobacillus-dominant state. Models (LEfSe, Random Forest) identified a marked reduction in pathobionts (Gardnerella, Sneathia, Prevotella) post-treatment. In the prospective cohort, the HR-HPV clearance rate reached 82.9% (29/35) after three menstrual cycles, synchronized with significant reductions in mean vaginal pH (4.85 ± 0.42 to 4.12 ± 0.35, p < 0.001) and an 85.7% Nugent score normalization rate. Crucially, Kushen Gel treatment was associated with a profound shift from a pro-inflammatory to an anti-viral immune microenvironment. Pro-inflammatory markers (IL-8, IL-6, TNF-α) plummeted significantly (p < 0.0001), while anti-viral IFN-γ exhibited a robust increase (3.2 ± 1.1 to 18.6 ± 5.4 pg./mL, p < 0.0001), particularly in responders. Lactobacillus abundance positively correlated with IFN-γ (r = 0.68) and inversely with IL-8 (r = -0.54). Kushen Gel is associated with HR-HPV clearance and concurrent vaginal microenvironment remodeling, marked by suppressed anaerobic-driven inflammation and an enhanced IFN-γ-associated anti-viral niche dominated by Lactobacillus. These findings biologically support using Kushen Gel to manage vaginal dysbiosis and HR-HPV regression.

PMID 42465087
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PubMedbioRxiv : the preprint server for biology2026-07-17

Tracing developmental and adult hematopoiesis with an endogenous zebrafish runx1-2A-CreERT2 CRISPR knock-in.

Preston James A JA, Usha Masuma K MK, Ekker Stephen C SC, Clark Karl J KJ et al.

Zebrafish combines the power of genetics and unparalleled in vivo imaging for investigating the dynamics of vertebrate hematopoietic development. Across species, the transcription factor Runx1 is essential for definitive hematopoiesis. We generated a zebrafish runx1-2A-creERT2 CRISPR knock-in for tamoxifen-regulated Cre recombinase Runx1 lineage tracing and characterized its activity using the ubi:Switch recombinase-dependent fluorescence reporter, microscopic live imaging and flow cytometry. Tamoxifen treatment beginning at gastrula stage labeled all expected Runx1 lineages in the early embryo, including neuroectodermal olfactory placode and Rohan-Beard neurons, primitive hematopoietic blood cells, and nascent hematopoietic stem and progenitor cells (HSPCs) in the dorsal aorta. Runx1 HSPCs colonized the larval caudal hematopoietic tissue and thymus from three to five days of development. Timed tamoxifen induction of Cre activity allowed separation of Runx1 primitive hematopoiesis from definitive HSPC emergence and larval stem cell niche colonization. Flow cytometry of kidney marrow and peripheral blood from adults treated with tamoxifen at gastrula stage revealed Runx1 embryonic hematopoietic cells contributed to adult hematopoietic precursors, myeloid, lymphoid, and peripheral blood lineages. Labeling of all blood lineages was also effective by tamoxifen treatment of 5-month-old adults. The zebrafish runx1-2A-creERT2 line provides a powerful tool for precise spatial and temporal analysis of Runx1 progenitor mechanisms in developmental and adult hematopoiesis. zebrafish endogenous runx1-2A-creERT2 provides inducible Cre recombinase genetic analysis in all runx1 neuromesodermal and blood lineages zebrafish runx1-2A-creERT2 line enables in vivo spatial and temporal analysis of embryonic and adult hematopoiesis.

PMID 42465524
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PubMedbioRxiv : the preprint server for biology2026-07-17

IFN γ and IFN γ mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.

Araveti Prasanna Babu PB, Yabaji Shivraj M SM, Arifin Muhammad Zainul MZ, Lata Suruchi S et al.

Type I interferons (IFN-I) and IFNγ exert divergent effects during tuberculosis, but the mechanisms that determine whether macrophage activation promotes host defense or inflammatory pathology remain incompletely understood. Here, we dissect the interplay between IFN-I and IFNγ in macrophage activation using genetically susceptible B6.Sst1S macrophages. We show that, during tumor necrosis factor (TNF) stimulation, susceptible macrophages enter a persistent pathological activation state (pPAS) characterized by sustained lipid peroxidation and super-induction of IFN-I responses. This pathological state is maintained by autocrine IFN-I signaling. In contrast, IFNγ priming prevents pPAS development by enhancing macrophage resilience to oxidative stress, in part through regulation of iron metabolism and induction of ferritin expression. Computational c ell s tate t ransition a ssessment and r egulation (cSTAR) analysis identified pathways and small molecules predicted to promote the transition of susceptible macrophages toward an IFNγ-induced, Mtb-resistant state. Consistent with these predictions, the CDK4/6 inhibitor trilaciclib reduced lipid peroxidation by regulating iron metabolism, whereas retinoic acid signaling enhanced GPX4 expression and lipid biosynthesis programs. Combined CDK4/6 inhibition and retinoic acid receptor activation efficiently prevented the pathological activation state. Together, these findings delineate a mechanism of IFN-I/IFNγ crosstalk during macrophage activation and identify pharmacologic strategies to prevent IFN-I-dominant, lipid peroxidation-driven macrophage pathology.

PMID 42465263
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