About

Shravan Dave is an Associate Clinical Professor in the Department of Medicine at UC San Diego. His research focuses on hepatology, with particular emphasis on hepatocellular carcinoma, liver transplantation, non-alcoholic fatty liver disease, and the effects of immune checkpoint inhibitors on liver outcomes. He has contributed to numerous publications in these areas, including validation studies, clinical trials, systematic reviews, and editorial articles. His work involves investigating the incidence, treatment, and outcomes of liver-related diseases, as well as exploring the efficacy of pharmacologic therapies and the impact of treatment strategies on post-transplant outcomes. Dr. Dave's research is characterized by a strong clinical trial component and a focus on translating findings into improved patient care.

Research topics

• Internal medicine
• Medicine
• Endocrinology
• Gastroenterology
• Pathology
• Biology
• Physiology
• Bioinformatics
• Immunology

Selected publications

• The HIV/HBV Co‑infection Paradox: Immune Modulation Amid Persistent Risk [Response To Letter]

  Infection and Drug Resistance · 2026-05-01

  articleOpen access

  We thank Peppa et al for their thoughtful response to our review and for contributing important emerging data on immune phenotypes in HIV/HBV co-infection.Their observations add valuable mechanistic insight, particularly by highlighting distinctions in immune remodeling between treated and untreated states of HIV/HBV co-infection in individuals receiving long-term HBV-active antiretroviral therapy.Such data are important for refining our understanding of host-virus interactions in the modern treatment era.We agree that the immunologic landscape of treated HIV/HBV co-infection is more complex than a uniformly detrimental model would imply.The reported findings of enhanced adaptive NK-cell activity and preserved HBV-specific CD8 + T-cell responses in well-characterized cohorts of individuals with HIV/HBV co-infection receiving long-term suppressive therapy are significant 1,2 and may help explain clinical observations such as higher rates of HBsAg clearance reported in people with co-infection following initiation of HBV-active ART. 3,4These findings appropriately emphasize that effective treatment can partially reshape immune dysfunction associated with chronic dual infection.However, extrapolation of these observations to imply a protective or advantageous state would be premature.Rather, they highlight context-dependent immune adaptation under conditions of sustained viral suppression, which does not negate the broader evidence of increased clinical risk.A substantial body of evidence continues to demonstrate that untreated or incompletely treated HIV/HBV co-infection is associated with greater immune dysregulation, accelerated liver disease, and worse long-term outcomes than either infection alone. [5][6]6][7] Importantly, our use of the term "synergistic reinforcement" was intended to reflect the overall biological and clinical trajectory across disease states, rather than a uniform immunologic phenotype under all treatment conditions.As Peppa et al note, co-infection is not benign.Comparable examples have been described in other chronic viral infections.In patients with HBV and HCV coinfection, the introduction of direct acting antivirals for hepatitis C led to reports of HBV reactivation, including severe and occasionally fatal cases, following rapid HCV clearance. 8This phenomenon likely reflects the removal of suppressive antiviral pathways induced during chronic HCV infection.Similarly, cytomegalovirus can enhance specific immune modulatory responses while simultaneously driving chronic inflammation, immune senescence, and end-organ disease, particularly in older adults and immunocompromised individuals. 9,10These examples demonstrate that measurable immune effects during co-infection do not necessarily translate into reduced clinical risk.The same principle applies to HIV/HBV co-infection in the tenofovir era.Although HBV-active antiretroviral therapy has markedly improved prognosis, 11 it is premature to conclude that fibrosis progression, hepatic decompensation, or liver-related mortality have normalized.Several longitudinal studies continue to show progression to advanced fibrosis or persistent cirrhosis in a subset of treated individuals, and fibrosis regression appears less pronounced than that reported in Infection and Drug Resistance 2026:19 621913 1

  PublisherOA PDFDOI

• Hepatic Viral Reservoirs in Concurrent HIV and HBV: From Mechanistic Insight to Integrated Cure Strategies

  Infection and Drug Resistance · 2026-03-01 · 1 citations

  articleOpen access

  Purpose of Review: Concurrent HIV and hepatitis B virus (HBV) affect an estimated 4– 5 million people worldwide and remain a major driver of liver-related morbidity and mortality, even among individuals receiving tenofovir-containing antiretroviral therapy (ART). Both viruses establish long-lived reservoirs that are not eliminated by current antiviral therapies. This review summarizes current mechanistic and clinical frameworks for understanding concurrent HIV and HBV, highlights the interplay between their viral reservoirs, and discusses the implications of these interactions for cure strategies. Recent Findings: The liver functions as a multicellular reservoir. HBV persists within hepatocytes as nuclear covalently closed circular DNA (cccDNA) and integrated viral sequences. HIV persists as integrated provirus in tissue-resident CD4⁺ T cells and liver macrophages, with evidence supporting viral transfer or cell-to-cell spread involving stellate cells and hepatocytes. Concurrent HIV and HBV accelerate fibrosis and immune dysfunction through shared pathogenic pathways, including epigenetic silencing, cytokine- and checkpoint-mediated T-cell exhaustion, metabolic stress, and inflammation driven by the gut–liver axis. HBV-associated liver injury promotes recruitment of HIV target cells, while HIV-associated immune dysregulation impairs HBV control. Despite these interlinked biological mechanisms, individuals living with HIV and HBV are frequently excluded from clinical trials, slowing therapeutic progress and exacerbating health inequities. Summary: Concurrent HIV and HBV represent a synergistic disease model that demands integrated therapeutic approaches and inclusive research frameworks. Priority needs include robust tissue-based reservoir measurements, validated biomarkers that distinguish latent from transcriptionally active viral states, combination strategies incorporating antiviral, antifibrotic, and immunomodulatory agents, and community-engaged clinical trial designs that are inclusive of individuals living with HIV and HBV and safe in the context of HBV. Advancing these areas will be essential to achieving durable remission—and ultimately functional cure—for both viruses. Plain Language Summary: HIV and hepatitis B virus (HBV) often occur together and affect millions of people worldwide. Both viruses can persist in the liver, forming “viral reservoirs” that current treatments cannot eliminate. These hidden viral reservoirs contribute to long-term liver damage, including scarring (fibrosis) and liver cancer. This review explains how HIV and HBV interact and reinforce each other’s persistence. We describe how different liver cells—including immune cells and hepatocytes—create an environment that allows both viruses to survive. We also highlight emerging scientific tools and treatment strategies designed to better target viral reservoirs. Importantly, people living with HIV and HBV are often excluded from research studies. Including these individuals in future clinical trials will be essential to develop fair and effective cures for both viruses. Keywords: HIV, hepatitis B virus, liver, viral reservoirs, persistence, cure strategies

  PublisherOA PDFDOI

• The HIV/HBV Co‑infection Paradox: Immune Modulation Amid Persistent Risk [Response To Letter]

  Dove Medical Press (Taylor and Francis Group) · 2026-05-14

  articleOpen access

  Renato Bobadilla,1 Finn MacLean,2 Shravan Dave,3 Jason T Blackard,4 Sara Gianella1 1Division of Infectious Diseases and Global Public Health, University of California San Diego, La Jolla, San Diego, CA, USA; 2Medical Scientist Training Program, University of California San Diego, La Jolla, San Diego, CA, USA; 3Division of Gastroenterology and Hepatology, University of California San Diego, La Jolla, San Diego, CA, USA; 4Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USACorrespondence: Sara Gianella, Division of Infectious Diseases and Global Public Health, University of California San Diego, 9500 Gilman Drive MC 0679, La Jolla, CA, 92093, USA, Email gianella@health.ucsd.edu

  Publisher

• Downstaging of hepatocellular carcinoma before liver transplantation: Results from a national multicenter prospective cohort study

  Hepatology · 2025-01-14 · 17 citations

  articleOpen access

  BACKGROUND AND AIMS: Patients with HCC meeting United Network for Organ Sharing (UNOS)-downstaging (DS) criteria have excellent post-liver transplantation (LT) outcomes. Studies on HCC beyond UNOS-DS criteria ("All-Comers" [AC]) have been limited by small sample size and short follow-up time, prompting this analysis. APPROACH AND RESULTS: Three hundred twenty-six patients meeting UNOS-DS and 190 meeting AC criteria from 9 LT centers across 5 UNOS regions were enrolled from 2015 to 2023 and prospectively followed. Competing risk analysis and Kaplan-Meier method were used to evaluate DS and LT outcomes, and Fine-and-Gray and Cox models were used to identify predictors of outcomes. AC and UNOS-DS had similar median alpha-fetoprotein (15 vs. 12 ng/mL; p =0.08), MELD (9 vs. 9; p =0.52), and Child-Pugh (A vs. A; p =0.30). Two years after the first local regional therapy, 82% of UNOS-DS and 66% of AC were successfully downstaged ( p <0.001). In AC, DS rates were 72% for tumor number plus diameter of largest lesion <10, 51% for sum 10-12, and 39% for sum >12 ( p =0.01). Yttrium-90 achieved higher DS success than transarterial chemoembolization in AC (74% vs. 65%; p <0.001). 48% of UNOS-DS and 40% of AC underwent LT ( p =0.10). Five-year post-LT survival was similar between UNOS-DS and AC (74% vs. 72%; p =0.77), although 5-year post-LT recurrence was higher in AC (30% vs. 14%; p =0.02). CONCLUSIONS: Despite higher HCC recurrence and lower intention-to-treat survival in AC, post-LT survival was comparable between UNOS-DS and AC. Yttrium-90 attained higher DS success than transarterial chemoembolization in AC. LT after DS is feasible in AC, though defining an upper limit in tumor burden may be necessary.

  PublisherOA PDFDOI

• A prospective multicenter validation of RETREAT for posttransplantation HCC recurrence prediction

  Hepatology · 2025-03-11 · 10 citations

  articleOpen access

  BACKGROUND AND AIMS: The RETREAT(Risk Estimation of Tumor REcurrence After Transplant) score is a simple risk stratification tool for postliver transplantation (LT) HCC recurrence that has been validated in retrospective cohort studies. A prospective, multicenter study is needed to further demonstrate accuracy especially given the evolving clinical demographics and HCC transplant practice. Our aim is to validate and compare the RETREAT score to other post-LT HCC recurrence risk scores in a contemporary, prospective cohort of patients. APPROACH AND RESULTS: We prospectively enrolled patients with HCC who underwent LT from 8 centers between 2018 and 2022. The primary outcome was post-LT recurrence-free survival. Secondary outcomes included post-LT and post-recurrence survival. Model performance, determined using the concordance index, Akaike information criterion, integrated Brier score, and calibration, was compared to that of other established risk scores.We included 1166 patients with HCC who underwent LT, of which 78 (6.7%) had post-LT HCC recurrence after a median follow-up time of 2.2 years (IQR 1.2-3.2). The median RETREAT score was 4 (IQR 3-5) in patients with post-LT HCC recurrence and 1 (IQR 1 - 2) in patients without. Those with a RETREAT score of 0, 3, and 5+ had a 99.4%, 84.1%, and 55.6% recurrence-free survival, respectively, at 3 years post-LT. The RETREAT score was also able to stratify post-LT overall and postrecurrence survival. The RETREAT score's concordance index was 0.81 (95% CI: 0.77-0.85) and outperformed the MORAL and RELAPSE scores across multiple metrics. CONCLUSIONS: The RETREAT score retains high accuracy for predicting post-LT HCC recurrence, further supporting RETREAT-guided post-LT HCC surveillance and care.

  PublisherOA PDFDOI

• Clinical Trial to Assess the Safety and Tolerability of Anti‐<scp>IL</scp> 23 Monoclonal Antibody Guselkumab in Patients With Alcohol‐Associated Liver Disease

  Alimentary Pharmacology & Therapeutics · 2025-02-14 · 4 citations

  articleOpen access

  BACKGROUND: There are no FDA-approved therapies for alcohol-associated liver disease (ALD). Preclinical studies indicate that blocking IL-23/IL-17 signalling may reverse liver injury. Guselkumab, an IL-23-specific antibody approved for psoriasis, may be beneficial for ALD. AIMS: We aimed to assess the safety and tolerability of guselkumab in patients with ALD. METHODS: This phase-1 dose-escalation study included patients with ≥ 2 DSM-5 criteria for alcohol use disorder, significant steatosis (MRI-PDFF ≥ 8%) and MRE < 3.63 kPa (to exclude advanced disease). Guselkumab was given subcutaneously on Days 1 and 29 in 30, 70 or 100 mg dose cohorts. Primary endpoints were adverse events (AEs) and dose-limiting toxicity. RESULTS: We enrolled 13 patients (three 30 mg, three 70 mg, and seven 100 mg). Eleven completed the study and two early discontinued in the 100 mg group. Of them, 77% were men, and the median age was 53 [IQR 49-61] years. The median MRI-PDFF and MRE were 18.4% [IQR 8.4%-34.0%] and 2.5 [2.2-2.6] kPa, respectively. The most frequent AEs were hyperuricemia (13%, mild only) and elevated lipase (11%, mild and moderate). There were no serious adverse events or significant variations in liver enzymes. There was a suppression of peripheral interleukin (IL)-17, IL-23, IL-1b and TNF-α in the 70 and 100 mg groups, and a significant decrease in alcohol consumption over time (AUDIT-C: 6 [3-7] vs. 5 [1-6], p = 0.023). CONCLUSIONS: Guselkumab is safe in doses up to 100 mg and may reduce inflammation markers in ALD. These findings support further phase 2 studies to evaluate the efficacy of guselkumab in ALD, particularly in patients with severe phenotypes.

  PublisherOA PDFDOI

• Tu1560: EVALUATING WAITLIST DROPOUT AND POST-LIVER TRANSPLANT OUTCOMES FOR PATIENTS WITH ALCOHOL-ASSOCIATED LIVER DISEASE AND CARDIOMETABOLIC COMORBIDITIES

  Gastroenterology · 2025-05-01

  article
  PublisherDOI

• Editorial: Checkpoint Inhibitor‐Induced Liver Injury—Time to Abandon <scp>CTCAE</scp>?

  Alimentary Pharmacology & Therapeutics · 2024-10-14 · 2 citations

  editorialOpen accessSenior authorCorresponding

  Immune checkpoint inhibitors (ICIs) are increasingly used in oncologic regimens for a wide variety of cancers with impressive improvement in patient outcomes. Checkpoint inhibitor-induced liver injury (CHILI) is one feared adverse effect of these treatments. CHILI can be heterogeneous in presentation, so it is essential to establish causality and grade the severity of injury to prognosticate and influence management [1]. The U.S. National Cancer Institute created the Common Terminology Criteria for Adverse Events (CTCAE) to grade the severity of injury from oncologic treatments [2]. However, this grading system was developed prior to the advent of widespread immunotherapy and may not adequately capture hepatic dysfunction [3]. Nonetheless, oncologic society guidelines advocate for the use of the CTCAE framework to manage ICI withdrawal and corticosteroid therapy. There is conflicting data on this approach, with some clinical evidence that patients may improve by stopping ICIs alone [4-6]. Among patients with grades 3 and 4 injury, guidelines advise against re-challenging with immunotherapy. There has been increased interest in using alternative grading scales such as the U.S. Drug-Induced Liver Injury Network (DILI-N) and the International DILI Expert Working Group (DILI-IEWG) to more accurately reflect degree of injury and guide treatment recommendations. Within this emerging context, Hountondji and colleagues examined patients with grades 3 and 4 CHILI as defined by the CTCAE system and compared their clinical characteristics, management and outcomes against the DILI-N and DILI-IEWG framework [7]. The authors demonstrate that the CTCAE scale categorises more patients with severe CHILI compared to the DILI-N or DILI-IEWG classifications. This suggests that the CTCAE framework may prematurely limit a therapeutic opportunity for patients after an episode of an otherwise minor CHILI. The authors demonstrate that the DILI-N and DILI-IEWG models are superior at predicting true liver dysfunction and 90-day mortality compared to CTCAE. Prior studies evaluating the scoring system for CHILI have found that CTCAE tends to overestimate the clinical severity of liver injury [1, 3]. This paper captures the key component of why DILI-N and DILI-IEWG are more sensitive grading systems compared to CTCAE—they account for true hepatic function by including INR and encephalopathy. The authors also compared these scoring systems to the venerable model for end-stage liver disease (MELD) to provide grounding. This paper advances the field by better defining CHILI outcomes in a key first step to further refine which patients currently classified as grade 3 or 4 via the CTCAE pathway may be safely re-challenged with ICIs. This is especially important given many of these patients have limited therapeutic options left. Most importantly, Hountondji et al. manage to utilise well-researched understanding of DILI within the field of hepatology to validate it in a new oncologic paradigm. We hope this will catalyse a movement towards an encouraging future for patients with advanced malignancy who suffer from CHILI. Kelly Torosian: writing – review and editing. Shravan Dave: writing – review and editing, conceptualization, supervision. This article is linked to Hountondji et al papers. To view these articles, visit https://doi.org/10.1111/apt.18276 and https://doi.org/10.1111/apt.18343. The data that supports the findings of this study are available in the supporting information of this article.

  PublisherOA PDFDOI

• Editorial: NAFLD, NAFLD, or MASLD: what's in a name?

  Alimentary Pharmacology & Therapeutics · 2024-08-13

  editorialOpen accessSenior authorCorresponding

  LINKED CONTENT This article is linked to Kim et al paper. To view this article, visit https://doi.org/10.1111/apt.18011

  PublisherOA PDFDOI

• Impact of pre-transplant immune checkpoint inhibitor use on post-transplant outcomes in HCC: A systematic review and individual patient data meta-analysis

  Journal of Hepatology · 2024-07-10 · 87 citations

  reviewOpen access
  PublisherOA PDFDOI

Frequent coauthors

• Rohit Loomba

  6 shared

• Manon Allaire

  Inserm

  5 shared

• Abdul M. Majzoub

  5 shared

• Abbey Barnard

  5 shared

• Beom Kyung Kim

  4 shared

• Panu K. Luukkonen

  4 shared

• Pranab Barman

  4 shared

• Zachary Gitto

  University of South Carolina

  4 shared

Education

• Ph.D., Molecular and Computational Biology

  University of California, San Diego

  2007

• M.S., Molecular and Computational Biology

  University of California, San Diego

  2003

• B.S., Molecular and Computational Biology

  University of California, San Diego

  2001