iPVD Consortium Publications and Events

Presentations

• Microbiome metabolite-driven modulation of PH – Imad Al Ghouleh, Department of Medicine, The Warren Alpert Medical School of Brown University, USA
• Update on presentations and mechanisms of sexual dimorphisms in the cardiopulmonary vascular system in PVD – Tim Lahm, University of Colorado Anschutz Medical Campus, National Jewish Health, USA 

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Presentations

• Co-Infection and PVD – Hanan Yusuf, Addis Ababa University College of Health Sciences, Ethiopia

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Presentations

• HIV and PH – Nicola Petrosillo, University Hospital Campus Bio-Medico, Italy

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Presentations

• Unveiling the burden: Post-tuberculosis PVD in South Africa Friedrich Thienemann, University of Cape Town, South Africa 

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Presentations

• Microbiome and pulmonary circulation: where are we going? (Moderator introduction) – Suellen D Oliveira, University of Illinois at Chicago, USA 
• Pro-inflammatory gut microbiome in PAH patients – Thenappan Thenappan, University of Minnesota, USA 
• Insights into the role of microbiome metabolites in PH – Imad Al Ghouleh, University of Pittsburgh, USA

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Presentations

• Echocardiographic screening and prognostic significance of PH – Simon Stewart, University of Notre Dame, Australia & Eduardo Mondlane University, Mozambique
• PH in children from low- and middle-income countries – Judith Namuyonga, Uganda Heart Institute, Uganda

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Presentations

• PH in the shadow of infections: challenges in Indian practice – Prashant Bobhate, Kokilaben Dhirubai Ambani Hospital, Mumbai, India 

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Presentations

• Beyond parasites and viruses - fungi & PH – Sharilyn Almodovar (Moderator), Texas Tech University, USA 
• Pulmonary paracoccidioidomycosis-induced PH – Alexandre Todorovic Fabro, University of São Paulo, Brazil

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Presentations

• When SARS-CoV-2 meets the pulmonary circulation – Navneet Dhillon (Moderator), University of Kansas, USA 
• Endothelial progenitor cells: A potential biomarker for evaluating endothelial health in post Covid patients – Olga Tura-Ceide, University of Barcelona, Spain

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Presentations

• Schistosomiasis-associated PAH – Rudolf Oliveira (Moderator), Federal University of São Paulo, Brazil 
• Schistosomiasis-associated PAH: when the Schisto camouflage fails – Brian Graham, University of San Francisco, USA

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Presentations

• Inaugural series - inflammation and the pulmonary circulation: the good, the bad and the ugly (moderator introduction) – Vinicio de Jesus Perez, Stanford University, USA 
• Adaptive immunity: role of Tregs in PAH – Rajkumar Savai, Max Planck Institute for Heart and Lung Research, Germany

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Presentations

• Inaugural series - inflammation and the pulmonary circulation: the good, the bad and the ugly – Peter Nyasulu, University of the Witwatersrand, South Africa 
• Inflammatory lung microenvironment in lung cancer-associated PH – Rajkumar Savai, Max Planck Institute for Heart and Lung Research, Germany

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Presentations

• Infection and PH - why have we started the iPVD Consortium? – Ghazwan Butrous, University of Kent, UK 
• Inaugural series - inflammation and the pulmonary circulation: the good, the bad and the ugly – Suellen Darc Oliveira, University of Illinois at Chicago, USA 
• scRNAseq reveals inflammatory EC phenotypes in PAH – Kewal Asosingh, Cleveland Clinic, USA

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Held during the PVRI 2026 Dublin, the meeting brought together international experts to discuss current challenges in diagnosing and managing infection-related PVD, particularly in low- and middle-income countries (LMICs). The programme explored clinical trial challenges, environmental stressors affecting the pulmonary vasculature, and new insights into the role of the microbiome in PVD.

Programme highlights

Session 1 – Challenges & opportunities in conducting PAH clinical trials in LMIC

• Highlights of the NIH Sch-PAH multicentre initiative – Brian Graham
• Advances in the clinical diagnosis of Sch-PAH – Camila Loureiro
• Pathways to diagnose iPVDs in rural areas – Ana Olga Mocumbi

Session 2 – Environmental stressors and iPVD

• The pulmonary vasculature at risk: pollution & PVD – Norbert Weissmann
• Extracellular vesicles, exposomes and HIV-associated PH – Navneet Dhillon
• The sleep, infection and PH triad – Andrew Bryant
• N-Ras: a novel player in endothelial & T cell pathophysiology in PH? – Edgar Fernández-Malavé

Session 3 – New advances in the role of microbiome in PVD pathophysiology

• Gut-lung crosstalk in Sch-PH – Suellen D’Arc Oliveira
• Microbiome as a treatment option in PAH – Thenappan Thenappan
• The link between microbiome, infection & PVD – Sharilyn Almodovar

Held during the PVRI 2025 Rio, the 4th iPVD Symposium focused strongly on schistosomiasis-associated PVD, one of the most important infectious causes of PH worldwide. Researchers and clinicians discussed new insights into diagnosis, disease mechanisms, epidemiology, and public health challenges.

Key discussion themes

Diagnosis and clinical challenges

• Differentiating schistosomiasis-associated PAH from idiopathic PAH remains difficult, particularly in endemic regions

• Accurate diagnosis often requires liver imaging, portal hypertension markers, and serology

Disease mechanisms

• Disease arises from a complex interaction between parasite burden, Th2-driven inflammation, and host genetic factors

Epidemiology

• Many cases are diagnosed years after migration from endemic regions

• Limited screening and clinical awareness continue to delay diagnosis

Future priorities

• Developing biomarkers for earlier detection

• Expanding echocardiographic and antigen-based screening

• Strengthening multidisciplinary and public health approaches

Held at PVRI 2022 Athens, the 3rd iPVD Symposium brought together international experts to discuss emerging research on infection and PVDs, with presentations spanning basic science, clinical research, and global health perspectives.

Held during PVRI 2020 Lima, the 2nd iPVD Symposium explored the complex relationship between infection, inflammation, and PVDs.

Programme highlights

Infection and PVD

• Infection, inflammation and immunology in pulmonary vascular pathology – Stephen Chan
• Epidemiology of schistosomiasis and HIV in Africa – Ana Mocumbi
• Spectrum of infectious diseases and PVD – Ghazwan Butrous

Schistosomiasis and PVD

• Pathogenesis of schistosomiasis-associated pulmonary vascular disease – Rahul Kumar
• Schistosoma japonicum and PVD – Brian Graham
• Clinical manifestations and management of PH due to schistosomiasis – Angela Bandeira and Rogério Souza

HIV and PVD

• Pulmonary vascular injury in HIV infection – Navneet Dhillon
• Pulmonary vascular pathology in HIV infection with drug abuse – Vinicio de Jesus Perez
• Clinical aspects of HIV-associated PH – Nicola Petrosillo

Other infections

• Microbiota and PH – Francisco Pérez-Vizcaíno
• Fungal infection and PVD – Alexandre Todorovic Fabro
• Tuberculosis-associated PVD – Gerald Maarman

The first international Symposium was held in Aswan, Egypt in 2019. This multidisciplinary meeting brought together cardiologists, pulmonologists, infectious disease specialists, immunologists, epidemiologists, and parasitologists to explore the role of infection in PVDs.

Key themes

• Inflammation and immune responses in PVD

• Schistosomiasis and other helminthic infections

• HIV-associated PVD

• Bacterial and fungal infections

• Coinfection, including HIV and schistosomiasis

• Epidemiology of infection-related PH

• Pharmacological interventions and treatment strategies

• Public health, education, and training needs

The Symposium helped raise awareness of the importance of infection in the development and progression of PVD and laid the foundation for the iPVD Consortium’s ongoing collaborative research efforts.

12 July 2025, 17(4):84

Andrea Jazel Rodríguez-Herrera, Sabrina Setembre Batah, Maria Júlia Faci do Marco, Carlos Mario González-Zambrano, Luciane Alarcão Dias-Melicio, Alexandre Todorovic Fabro

Abstract

Background/Objective
Pulmonary fungal infections are a significant diagnostic challenge, primarily affecting immunocompromised individuals, such as those with HIV, cancer, or organ transplants, and they often lead to substantial morbidity and mortality if untreated. These infections trigger acute inflammatory and immune responses, which may progress to chronic inflammation. This process involves myofibroblast recruitment, the deposition of extracellular matrix, and vascular remodeling, ultimately contributing to pulmonary hypertension. Despite its clinical relevance, pulmonary hypertension secondary to fungal infections remains under-recognized in practice and poorly studied in research. 

Results/Conclusion
This narrative mini-review explores three key mechanisms underlying vascular remodeling in this context: (1) endothelial injury caused by fungal emboli or autoimmune reactions, (2) direct vascular remodeling during chronic infection driven by inflammation and fibrosis, and (3) distant vascular remodeling post-infection, as seen in granulomatous diseases like paracoccidioidomycosis. Further research and clinical screening for pulmonary hypertension in fungal infections are crucial to improving patient outcomes.

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9 Jun 2025, 17(3):66

Sasha Z Prisco, Suellen D Oliveira, E Kenneth Weir, Thenappan Thenappan, Imad Al Ghouleh

Abstract

Pulmonary arterial hypertension (PAH) is an irreversible disease characterized by vascular and systemic inflammation, ultimately leading to right ventricular failure. There is a great need for adjunctive therapies to extend survival for PAH patients. The gut microbiome influences the host immune system and is a potential novel target for PAH treatment. We review the emerging preclinical and clinical evidence which strongly suggests that there is gut dysbiosis in PAH and that alterations in the gut microbiome may either initiate or facilitate the progression of PAH by modifying systemic immune responses. We also outline approaches to modify the intestinal microbiome and delineate some practical challenges that may impact efforts to translate preclinical microbiome findings to PAH patients. Finally, we briefly describe studies that demonstrate contributions of infections to PAH pathogenesis. We hope that this review will propel further investigations into the mechanisms by which gut dysbiosis impacts PAH and/or right ventricular function, approaches to modify the gut microbiome, and the impact of infections on PAH development or progression.

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6 Jun 2025, 17(3):65

Amanda K Garcia, Noelia C Lujea, Javaria Baig, Eli Heath, Minh T Nguyen, Mario Rodriguez, Preston Campbell, Isabel Castro Piedras, Edu Suarez Martinez, Sharilyn Almodovar

Abstract

Background
Human Immunodeficiency Virus (HIV) infections remain a source of cardiopulmonary complications among people receiving antiretroviral therapy. Still to this day, pulmonary hypertension (PH) severely affects the prognosis in this patient population. The persistent expression of HIV proteins, even during viral suppression, has been implicated in vascular dysfunction; however, little is known about the specific effects of these proteins on the pulmonary vasculature. This study investigates the impact of Nef variants derived from HIV-positive pulmonary hypertensive and normotensive donors on pulmonary vascular cells in vitro. 

Methods
We utilized well-characterized Nef molecular constructs to examine their effects on cell adhesion molecule gene expression (ICAM1, VCAM1, and SELE), pro-apoptotic gene expression (BAX, BAK), and vasoconstrictive endothelin-1 (EDN1) gene expression in endothelial nitric oxide synthase (eNOS) nitric oxide and the production and secretion of pro-inflammatory cytokines over 24, 48, and 72 h post-transfections with Nef variants. 

Results
HIV Nef variants SF2, NA7, and PH-associated Fr17 and 3236 induced a significant increase in adhesion molecule gene expression of ICAM1, VCAM1, and SELE. Pulmonary normotensive Nef 1138 decreased ICAM1 gene expression, but had increased VCAM1. PH Nef ItVR showed a consistent decrease in ICAM1 and no changes in SELE and VCAM1 expression. Further gene expression analyses of pro-apoptotic genes BAX and BAK demonstrated that Nef NA7, SF2, normotensive Nef 1138, and PH Nef Fr8, Fr9, Fr17, and 3236 variants significantly increased gene expression for apoptosis. Normotensive Nef 1138, as well as PH Nef Fr9 and ItVR, all displayed a statistically significant decrease in BAX expression. The expression of EDN1 had a statistically significant increase in samples treated with Nef NA7, SF2, normotensive Nef 2044 and PH Nef 3236, Fr17, and Fr8. Notably, PH-associated Nef variants sustained pro-inflammatory cytokine production, including IL-2, IL-4, and TNFα, while anti-inflammatory cytokine levels remained insufficient. Furthermore, eNOS was transiently upregulated by all Nef variants except for normotensive Nef 2044. 

Conclusions
The distinct effects of Nef variants on pulmonary vascular cell biology highlight the complex interplay between Nef, host factors, and vascular pathogenesis according to the variants.

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17 April 2025, 17(2):35

Ghazwan Butrous

Abstract

Introduction
Infectious diseases significantly impact pulmonary vascular disorders, particularly in developing countries where parasitic infections remain prevalent. These infections constitute a substantial yet frequently overlooked contributor to pulmonary hypertension. 

Discussion
This review examines the prevalence of parasitic lung diseases in regions where communicable infections are endemic and highlights their pathophysiological links to pulmonary hypertension. Schistosomiasis and HIV notably increase pulmonary hypertension risk in these areas. While other infectious diseases may also cause pulmonary vascular lesions, most remain insufficiently studied. The review addresses global epidemiological trends, diagnostic challenges, and recent advancements in understanding the multifaceted origins of pulmonary hypertension. 

Conclusion
The association between parasitic infections and pulmonary hypertension is significant, necessitating a high index of suspicion for pulmonary hypertension in patients with a history of parasitic diseases, especially in endemic regions. More research is needed to understand infection-related pulmonary hypertension mechanisms and reduce its global impact.

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4 Mar 2025, 17(2):22

Camila M C Loureiro, André L Scheibler Filho, Vitor M A S Menezes, Ricardo A Correa, Rudolf K F Oliveira, Claudia Mickael, Joan F Hilton, Brian B Graham

Abstract

Background
Schistosoma-associated pulmonary arterial hypertension (Sch-PAH), a complication of hepatosplenic schistosomiasis, is still underdiagnosed and undertreated. Sch-PAH is the third-most common cause of pulmonary arterial hypertension (PAH) in Brazil, and it is estimated that there are around 60,000 afflicted individuals. However, there is a lack of data on these patients, especially in endemic areas. Therefore, this study aimed to describe baseline demographic data, hemodynamic severity of disease, and functional impairment of Sch-PAH patients at diagnosis.

Methods
For this systematic review, five databases (Embase, PubMed, SciELO, LILACS, and Cochrane) were searched to identify candidate publications reporting clinical, hemodynamic, and functional data at diagnosis of Sch-PAH patients referred to a PAH reference center in Brazil. Studies were excluded if they enrolled patients under the age of 18, the diagnosis was not confirmed by right heart catheterization (RHC), consisted of case reports, or did not report original data. Risk of bias was assessed using the Newcastle-Ottawa Scale and an adapted version for cross-sectional studies. Single-arm meta-analysis with a random-effect model was performed for each variable.

Results
From 459 studies identified through systematic database searching, five studies were selected for this meta-analysis. The majority of the included patients were women (67%), New York Heart Association (NYHA) functional class III/IV (57%), mean age 49 years (95% confidence interval [95% CI], 46-52), 6 min walk distance 392 m (95% CI, 291-493), mean pulmonary arterial pressure (mPAP) 59 mmHg (95% CI, 56-61), pulmonary vascular resistance (PVR) 12 WU (95% CI, 11-13) and cardiac index (CI) 2.57 L/min/m2 (95% CI, 2.25-2.88).

Conclusions
In summary, Sch-PAH has clinical characteristics similar to other forms of PAH, including connective tissue disease and idiopathic PAH. Additional studies or a unified registry would be essential for a better understanding of this relevant disease in Brazil.

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28 Feb 2025, 17(2):21

Chrisstoffel Jumaar, Steve Jacobs, Carmen Payne, Olakunle Sanni, Elize Louw, Nicola Baines, David Maree, Benjamin Botha, Merga Belina Feyasa, Hans Strijdom, Brian Allwood, Gerald J Maarman

Abstract

Background
Despite “successful” treatment, some lung tuberculosis (TB) patients develop long-term lung impairments that includes damage to the parenchyma and reduced function, which may predispose them to diseases like pulmonary hypertension. However, this is not well understood. Therefore, we investigated whether previous or current TB patients would display elevated biomarkers of endothelial dysfunction and vascular remodeling. 

Methods
We performed assays for ADMA, VCAM-1, VEGF, angiopoietin-1, TBARS, NT-pro-BNP, and cardiac troponin-I.We further stratified the patients based on 1, 2, 3, and >3 previous TB episodes, and 1–5 yrs, 5–10 yrs, 10–15 yrs and >15 yrs after the last TB treatment completion. We also assessed correlations between the biomarkers and the number of previous TB episodes or the time since the completion of the last TB treatment.

Results
ADMA was 70 times higher, VEGF was 2000 times higher and angiopoietin-1 was 6500 times higher than the normal range. NT-pro-BNP and cardiac troponin-I were undetected, and TBARS levels were low. There was a positive linear relationship between the number of previous TB episodes and angiopoietin-1, and between VEGF and the number of previous TB episodes. ADMA, VCAM-1 and TBARS exhibited a weak and negative linear association with the number of previous TB episodes. A negligible negative linear association was observed between the time since the completion of the last TB treatment and angiopoietin-1, VEGF and ADMA. 

Conclusions
Therefore, having >1 previous TB episode, despite the successful completion of TB treatment, associates with an increased risk of endothelial dysfunction/angiogenesis or vascular remodeling.

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27 Feb 2025, 17(2):19

Peter S Nyasulu, Jacques L Tamuzi, Rudolf K F Oliveira, Suellen D Oliveira, Nicola Petrosillo, Vinicio de Jesus Perez, Navneet Dhillon, Ghazwan Butrous

Abstract

Background/Objectives
Before the Coronavirus disease 2019 (COVID-19) era, the global prevalence of pulmonary arterial hypertension (PAH) was between 0.4 and 1.4 per 100,000 people. The long-term effects of protracted COVID-19 associated with pulmonary vascular disease (PVD) risk factors may increase this prevalence. According to preliminary data, the exact prevalence of early estimates places the prevalence of PVD in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection at 22%, although its predictive value remains unknown. PVD caused by COVID-19 co-infections is understudied and underreported, and its future impact is unclear. However, due to COVID-19/co-infection pathophysiological effects on pulmonary vascularization, PVD mortality and morbidity may impose a genuine concern-both now and in the near future. Based on reported studies, this literature review focused on the potential link between COVID-19, parasitic co-infection, and PVD. This review article also highlights hypothetical pathophysiological mechanisms between COVID-19 and parasitic co-infection that could trigger PVD.

Methods
We conducted a systematic literature review (SLR) searching peer-reviewed articles, including link between COVID-19, parasitic co-infection, and PVD. 

Results
This review hypothesized that multiple pathways associated with pathogens such as underlying schistosomiasis, human immunodeficiency virus (HIV), pulmonary tuberculosis (PTB), pulmonary aspergillosis, Wuchereria bancrofti, Clonorchis sinensis, paracoccidioidomycosis, human herpesvirus 8, and scrub typhus coupled with acute or long COVID-19, may increase the burden of PVD and worsen its mortality in the future. 

Conclusions
Further experimental studies are also needed to determine pathophysiological pathways between PVD and a history of COVID-19/co-infections.

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13 Feb 2025, 17(1):15

Sana Ayyoub, Navneet Kaur Dhillon, Olga Tura-Ceide

Abstract

Background/ Objectives
Long COVID or post-acute sequelae of SARS-CoV-2 infection (PASC) are symptoms that manifest despite passing the acute infection phase. These manifestations encompass a wide range of symptoms, the most common being fatigue, shortness of breath, and cognitive dysfunction. Genetic predisposition is clearly involved in the susceptibility of individuals to developing these persistent symptoms and the variation in the severity and forms. This review summarizes the role of genetic factors and gene polymorphisms in the development of major pulmonary vascular disorders associated with long COVID. 

Methods
A comprehensive review of current literature was conducted to examine the genetic contributions to pulmonary complications following SARS-CoV-2 infection. Studies investigating genetic polymorphisms linked to pulmonary hypertension, pulmonary thromboembolism, and pulmonary vascular endothelialitis were reviewed and summarized. 

Results
Findings show that specific genetic variants contribute to increased susceptibility to pulmonary vascular complications in long COVID patients. Variants associated with endothelial dysfunction, coagulation pathways, and inflammatory responses have been implicated in the development of pulmonary hypertension and thromboembolic events. Genetic predispositions influencing vascular integrity and immune responses appear to influence disease severity and progression. 

Conclusions
Understanding these mechanisms and genetic predispositions could pave the way for targeted therapeutic interventions to alleviate the burden on patients experiencing long COVID.

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10 Jan 2025, 17(1):5

Eloara V M Ferreira, Rudolf K F Oliveira, Reinaldo Salomao, Milena K C Brunialti, Martyella B A Cardoso, Chien-Nien Chen, Lan Zhao, Colm McCabe

Abstract

Background
Glucagon-like peptide-1 (GLP-1) agonists are an existing treatment option for patients with insulin-resistant states, which elicit further pleiotropic effects related to immune cell recruitment and vascular inflammation. GLP-1 agonists downregulate the cluster of differentiation 147 (CD147) receptor, one of several receptors for the SARS-CoV-2 spike protein that mediate viral infection of host cells.

Methods
We conducted an open-label prospective safety and tolerability study including biomarker responses of the GLP-1 agonist Liraglutide, administered for 5 days as an add-on therapy to the standard of care within 48 h of presentation in a cohort of 13 patients hospitalized with COVID-19 pneumonia. Biomarker responses were compared in patients admitted to critical care and those not requiring critical care admission (non-critical group).

Results
Liraglutide (0.6 mg, subcutaneously) was well tolerated by all patients and all patients were alive 30 days after diagnosis. Plasma soluble CD147 levels were reduced in the non-critical patient group at day 5 in contrast to critical care-treated patients, who demonstrated an increase in soluble CD147 levels between day 0 and day 5. Patients with milder COVID-19 pneumonia severity also demonstrated improvement in echocardiographic parameters of right and left ventricular function, reduction in plasma Troponin levels, increased CD147 expression on T lymphocytes, and reduction in plasma IL-8.

Conclusions
This first-in-disease use of the GLP-1 agonist Liraglutide demonstrates its safety and tolerability in an unselected cohort of patients hospitalized with COVID-19 pneumonia across a range of clinical severities.

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12 Nov 2024, 14(4), e70003

S. D. Oliveira, S. Almodóvar, G. Butrous, V De Jesus Perez, A. Fabro, B. B. Graham, A. Mocumbi, P. S. Nyasulu, O. Tura-Ceide, R. K. F. Oliveira, N. K. Dhillon

Abstract

Leveraging the potential of virtual platforms in the post-COVID-19 era, the Infection and Pulmonary Vascular Diseases Consortium (iPVDc), with the support of the Pulmonary Vascular Research Institute (PVRI), launched a globally accessible educational program to highlight top-notch research on inflammation and infectious diseases affecting the lung vasculature. This innovative virtual series has already successfully brought together distinguished investigators across five continents – Asia, Europe, South and North America, and Africa. Moreover, these open global forums have contributed to a comprehensive understanding of the complex interplay among immunology, inflammation, infection, and cardiopulmonary health, especially concerning pulmonary hypertension and related pulmonary disorders. These enlightening discussions have not only heightened awareness about the impact of various pathogenic microorganisms, including fungi, parasites, and viruses, on the onset and development of pulmonary vascular diseases but have also cast a spotlight on co-infections and neglected illnesses like schistosomiasis - a disease that continues to impose a heavy socioeconomic burden in numerous regions worldwide. Thus, the overall goal of this review article is to present the most recent breakthroughs from infectious PVDs as well as bring to light the scientific and educational insights from the 2023 iPVDc/PVRI virtual symposium series, shaping our understanding of these crucial health issues in this more than ever interconnected world.

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12 Jan 2023, 19(1)

Rahul Kumar, Öznur Aktay-Cetin, Vaughn Craddock, Daniel Morales-Cano, Djuro Kosanovic, Angel Cogolludo, Francisco Perez-Vizcaino, Sergey Avdeev, Ashok Kumar, Anil Kumar Ram, Stuti Agarwal, Ananya Chakraborty, Rajkumar Savai, Vinicio de Jesus Perez, Brian B Graham, Ghazwan Butrous, Navneet K Dhillon

Abstract

The Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and its sublineages pose a new challenge to healthcare systems worldwide due to its ability to efficiently spread in immunized populations and its resistance to currently available therapies. COVID-19, although targeting primarily the respiratory system, is also now well established that later affects every organ in the body. Most importantly, despite the available therapy and vaccine-elicited protection, the long-term consequences of viral infection in breakthrough and asymptomatic individuals are areas of concern. In the past two years, investigators accumulated evidence on how the virus triggers our immune system and the molecular signals involved in the cross-talk between immune cells and structural cells in the pulmonary vasculature to drive pathological lung complications such as endothelial dysfunction and thrombosis. In the review, we emphasize recent updates on the pathophysiological inflammatory and immune responses associated with SARS-CoV-2 infection and their potential long-term consequences that may consequently lead to the development of pulmonary vascular diseases.

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30 Nov 2022, 9:1041236

Rudolf K F Oliveira, Peter S Nyasulu, Adeel Ahmed Iqbal, Muhammad Hamdan Gul 4, Eloara V M Ferreira, John William Leclair, Zin Mar Htun, Luke S Howard, Ana O Mocumbi, Andrew J Bryant, Jacques L Tamuzi, Sergey Avdeev, Nicola Petrosillo, Ahmed Hassan, Ghazwan Butrous, Vinicio de Jesus Perez 

Abstract

COVID-19 infection primarily targets the lungs, which in severe cases progresses to cytokine storm, acute respiratory distress syndrome, multiorgan dysfunction, and shock. Survivors are now presenting evidence of cardiopulmonary sequelae such as persistent right ventricular dysfunction, chronic thrombosis, lung fibrosis, and pulmonary hypertension. This review will summarize the current knowledge on long-term cardiopulmonary sequelae of COVID-19 and provide a framework for approaching the diagnosis and management of these entities. We will also identify research priorities to address areas of uncertainty and improve the quality of care provided to these patients.

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19 May 2022, 19(5):314-331

Sarah Halawa, Soni S Pullamsetti, Charles R M Bangham, Kurt R Stenmark, Peter Dorfmüller, Maria G Frid, Ghazwan Butrous, Nick W Morrell, Vinicio A de Jesus Perez, David I Stuart, Kevin O'Gallagher, Ajay M Shah, Yasmine Aguib, Magdi H Yacoub

Abstract

The lungs are the primary target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, with severe hypoxia being the cause of death in the most critical cases. Coronavirus disease 2019 (COVID-19) is extremely heterogeneous in terms of severity, clinical phenotype and, importantly, global distribution. Although the majority of affected patients recover from the acute infection, many continue to suffer from late sequelae affecting various organs, including the lungs. The role of the pulmonary vascular system during the acute and chronic stages of COVID-19 has not been adequately studied. A thorough understanding of the origins and dynamic behaviour of the SARS-CoV-2 virus and the potential causes of heterogeneity in COVID-19 is essential for anticipating and treating the disease, in both the acute and the chronic stages, including the development of chronic pulmonary hypertension. Both COVID-19 and chronic pulmonary hypertension have assumed global dimensions, with potential complex interactions. In this Review, we present an update on the origins and behaviour of the SARS-CoV-2 virus and discuss the potential causes of the heterogeneity of COVID-19. In addition, we summarize the pathobiology of COVID-19, with an emphasis on the role of the pulmonary vasculature, both in the acute stage and in terms of the potential for developing chronic pulmonary hypertension. We hope that the information presented in this Review will help in the development of strategies for the prevention and treatment of the continuing COVID-19 pandemic.

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