Direct‐Acting Antiviral Treatment Failure and Retreatment Strategies Following Hepatitis C‐Positive Solid Organ Transplantation in Hepatitis C‐Negative Recipients: A Multicenter Case Series

ABSTRACT

Background

Transplanting solid organs from hepatitis C virus (HCV) nucleic acid testing (NAT+) donors (D+) into HCV‐negative recipients (R−) has become more common with the development of curative direct‐acting antiviral (DAA) treatment. Limited information exists to guide retreatment strategies for patients not achieving sustained virologic response (SVR) with DAAs. This multisite case series examines retreatment strategies and subsequent SVR rates in HCV‐negative solid‐organ transplant (SOT) recipients who did not achieve SVR following reactive initial DAA therapy following NAT+ SOT.

Methods

A retrospective multisite case series was conducted on patients not achieving SVR with initial DAA treatment post‐NAT+ HCV SOT between September 2016 and September 2022 across four tertiary medical centers in the United States.

Results

Thirteen patients were identified, predominantly receiving HCV NAT+ kidneys (77%) and SOF/VEL for 12 weeks as initial DAA therapy (43%). Baseline resistance testing was not performed. Median time to treatment initiation post‐SOT was 35 [IQR 22–41] days, and to retreatment postpositive viral load was 35 days [IQR 17–76]. Most patients (62%) were retreated with sofosbuvir/velpatasvir/voxilaprevir (SOF/VEL/VOX) for 12 weeks. Two patients required retreatment extension with SOF/VEL/VOX and SOF/VEL/VOX + ribavirin (RBV) from 12 to 24 weeks due to persistent viremia. Only one patient did not achieve SVR following retreatment with SOF/VEL/VOX for 12 weeks but did achieve SVR after a third course of treatment with SOF + GLE/PIB + RBV for 24 weeks.

Conclusion

Despite initial DAA failures, all HCV‐negative SOT recipients achieved SVR following one or more courses of retreatment with DAAs.

A multicenter, retrospective case series describes the population of hepatitis C virus (HCV) donor+/ recipient− (D+/R−) solid organ transplant (SOT) recipients failing an initial direct‐acting antiviral (DAA). Retreatment strategies and subsequent sustained virologic response (SVR) rates are reported. All patients achieved SVR following one or two retreatment courses.

Abbreviations

AASLD

American Association for the Study of Liver Diseases

ALT

alanine aminotransferase

AST

aspartate aminotransferase

D+

nucleic‐acid testing positive hepatitis C donor

DAAs

direct‐acting antivirals

DDI

drug/drug interaction

EMR

electronic medical record

GLE/PIB

glecaprevir/pibrentasvir

GT

genotype

HCV

hepatitis C virus

IDSA

Infectious Diseases Society of America

IQR

interquartile range

LDV/SOF

ledipasvir/sofosbuvir

N/A

not available

NAT+

nucleic‐acid testing positive

R−

hepatitis C negative recipient

RAS

resistance‐associated substitution

RBV

ribavirin

REDCap

Research Electronic Data Capture

SOF

sofosbuvir

SOF/VEL

sofosbuvir/velpatasvir

SOF/VEL/VOX

sofosbuvir/velpatasvir/voxilaprevir

SOT

solid organ transplant

SVR

sustained virologic response

VUMC

Vanderbilt University Medical Center

1. Introduction

In the United States, there is large disparity between patients in need of solid organ transplantation (SOT) and available donor organs [1, 2, 3, 4]. Historically, organs from hepatitis C virus (HCV) positive donors were discarded because HCV treatment with interferon, which is not recommended in SOT recipients, leads to poorer outcomes [5]. However, the advent of safe and effective direct‐acting antivirals (DAAs) for the treatment of HCV has allowed transplant centers to begin transplanting nucleic‐acid testing positive (NAT+) HCV donor (D+) organs into HCV‐negative recipients (R−). This expansion aims to increase access to transplantation, reduce SOT waitlist times and related mortality, while maintaining similar rates of posttransplant rejection and early mortality [6, 7, 8, 9].

Study variability exists in treatment regimens and timing of DAA initiation following HCV D+/R− SOTs, which can be categorized as prophylactic/preemptive (DAA initiation perioperatively without confirmation of viremia), or reactive (DAA initiation following confirmation of viremia). Despite this heterogeneity, sustained virologic response (SVR) rates are consistently near 100% for each approach [10, 11, 12, 13, 14, 15, 16]. In addition, little guidance exists for retreatment in cases where SVR is not achieved in this population. This case series compiles data from multiple sites to better describe the population of HCV D+/R− SOTs failing initial DAA therapy, report retreatment strategies and subsequent SVR rates.

2. Methods

2.1. Study Design

This retrospective case series of patients who failed to achieve SVR with initial DAA treatment following HCV D+/R− SOT between September 1, 2016 and September 30, 2022 was conducted at four tertiary medical centers in the United States. During this period, roughly 817 HCV D+/R− SOTs were completed: 421 kidneys, 200 livers, 157 hearts, 40 lungs, and 2 pancreases. All sites utilize a pharmacist to assist with DAA insurance authorization, financial assistance, and potential drug/drug interaction (DDI) monitoring. All patients received reactive DAA treatment following clinical stability, insurance authorization, and hospital discharge. Resistance‐associated substitution (RAS) testing was not assessed prior to initial DAA treatment. All patients experiencing HCV RNA increase after DAA initiation or not achieving an undetectable HCV RNA ≥ 12 weeks after DAA completion were included.

This study was approved by the Vanderbilt University Medical Center (VUMC) Institutional Review Board (#221687). Review was not required by Ochsner Health, the Medical University of South Carolina, or the University of Rochester. Data were retrospectively collected from the electronic medical record (EMR) and stored into Research Electronic Data Capture (REDCap) hosted at VUMC [17].

Baseline patient demographics including age, race, gender, SOT type, HCV genotype (GT), cirrhosis status, HCV RNA, HIV status, hepatitis B serologies, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were collected. Cirrhosis was defined as meeting any of the following: ultrasound demonstrating anatomical changes consistent with cirrhosis, liver biopsy with Metavir score F4, FIB‐4 score ≥ 3.25, APRI score ≥ 1.0, or transient elastography predicting F3‐F4 or F4 fibrosis. ALT normalization was defined as ≤ 33 U/L (males) and ≤ 25 U/L (females). Additional data collected included initial and subsequent DAA regimen(s), patient‐reported missed doses, on treatment and posttreatment HCV RNA, AST and ALT, time from SOT to DAA initiation and from DAA failure to DAA retreatment, RASs, and concomitant medications with potential to interact with prescribed DAA. SVR was defined as an undetectable HCV RNA ≥ 12 weeks following completion of DAA. Nonresponse was defined by an increase in HCV RNA while on DAA. Relapse was defined as detectable HCV RNA following undetectable HCV RNA without evidence of reinfection. Patients with initial HCV RNA decline without repeat HCV RNA available were considered relapsers in this series. Potential DAA medication interactions were identified and managed based on recommendations provided by the University of Liverpool HEP Drug Interaction Checker [18].

2.2. Endpoints and Statistical Analysis

Data were summarized using descriptive statistics, including median and range for continuous variables and frequency tabulations and percentages for categorical variables. The primary outcome was efficacy of DAA retreatment, defined by SVR achievement. Secondary endpoints were to describe the patient population and subsequent retreatment strategies.

3. Results

3.1. Patient Characteristics

Thirteen D+/R− SOT patients were included and found in Table 1. The median age was 57 years [interquartile range (IQR) 43–65] with most patients being White (62%; 8/13) males (77%; 10/13). The most common SOT type was kidney (77%; 10/13), followed by heart (8%; 1/13), liver (8%; 1/13), and lung (8%; 1/13). GT 1 HCV was most prevalent (62%; 8/13), followed by GT 3 (31%; 4/13) and GT 2 (8% 1/13). No patients had cirrhosis, HIV, hepatitis B virus, or baseline RAS testing.

TABLE 1.

Patient characteristics, DAA treatment regimens, DDIs, and outcomes.

ID	Gender	Race	Age	SOT type	GT	Baseline a HCV RNA (IU/mL)	Initial DAA treatment	Reported missed doses	Potential drug/drug interactions	Initial DAA treatment outcome	RAS Post initial DAA	DAA retreatment	Reported missed doses	Potential drug/drug interactions	DAA retreatment outcome
1	Male	White	73	Kidney	1	55 100 000	SOF/VEL ×12 weeks	0	Atorvastatin 20 mg daily​ Famotidine 40 mg daily​ Magnesium oxide 400 mg daily​ Tacrolimus 1.5 mg BID​	+viral load 4 weeks post EOT	Y93N	GLE/PIB + RBV ×16 weeks	0	Famotidine 20 mg BID​ Pravastatin 20 mg daily​ Tacrolimus 0.5 mg QAM and 1 mg QPM​	Achieved SVR34
2	Male	White	70	Kidney	1a	142 024	LDV/SOF ×12 weeks	0	Atorvastatin 20 mg daily​ Magnesium oxide 400 mg BID​ Omeprazole 20 mg daily​ Tacrolimus 2 mg BID​	+viral load 4 weeks post EOT	N/A	SOF/VEL/VOX ×12 weeks	1	Famotidine 20 mg daily​ Magnesium oxide 400 mg BID ​ Pravastatin 40 mg daily​ Tacrolimus 1 mg BID​	Achieved SVR41
3	Female	Black	69	Kidney	1a	333 196	SOF/VEL ×12 weeks	0	Famotidine 20 mg BID ​ Pravastatin 40 mg daily​ Sodium bicarbonate 650 mg BID​ Tacrolimus 8 mg BID​	+viral load 9 weeks post EOT	N/A	SOF/VEL/VOX ×12 weeks	0	Famotidine 20 mg BID​ Magnesium oxide 400 mg BID​ Pravastatin 40 mg daily​ Sodium bicarbonate 1300 mg BID​ Tacrolimus 8 mg QAM and 7 mg QPM​	Achieved SVR98
4	Female	White	63	Kidney	1a	4460	SOF/VEL ×12 weeks	0	Atorvastatin 20 mg daily​ Warfarin 5 mg daily Tacrolimus 4 mg BID​	+viral load 5 weeks post EOT	N/A	SOF/VEL/VOX ×12 weeks	0	Warfarin 5 mg daily​	Achieved SVR13
5	Male	Black	44	Kidney	1a	335 468	GLE/PIB ×12 weeks	0	Tacrolimus 5–7 mg BID​	+viral load increased while on GLE/PIB (GLE/PIB stopped Week 11) b	K24R M28G Q30R	SOF/VEL/VOX + RBV ×12 weeks	0	Intermittent famotidine 20 mg daily ​ Tacrolimus 6–7 mg BID​	Achieved SVR25
6	Male	Black	47	Kidney	1a	32 601	SOF/VEL ×12 weeks	0	Famotidine 20 mg daily​ Sodium bicarbonate 650 mg BID​ Tacrolimus 6–7 mg BID​	+viral load at EOT	N/A	SOF/VEL/VOX ×12 weeks	0	Famotidine 20 mg daily​ Sodium bicarbonate 650 mg BID​ Tacrolimus 6–7 mg BID​	Achieved SVR38
7	Male	Black	42	Kidney	2	1 766 004	GLE/PIB ×12 weeks	0	Pantoprazole 20 mg daily​ Tacrolimus 7 mg BID​	+viral load Week 9 (GLE/PIB stopped Week 10) c	N/A	SOF/VEL/VOX ×12 weeks	0	Famotidine 20 mg daily​ Sodium bicarbonate 1300 mg BID​ Tacrolimus 7 mg BID​	Achieved SVR24
8	Male	White	57	Kidney	3	> 25 000 000	GLE/PIB ×12 weeks	0	Carvedilol 25 mg BID​ Famotidine 20 mg daily​ Oxycodone 5 mg Q6H PRN​ Tacrolimus 2 mg BID​	+viral load 3 weeks post EOT	M28I/K L31L/P	SOF/VEL/VOX + RBV ×24 weeks d	7	Carvedilol 25 mg BID​ Famotidine 20 mg daily​ Magnesium oxide 400 mg daily​ Rosuvastatin for 14 days then changed to pravastatin 40 mg daily Tacrolimus 1.5 mg BID​	Achieved SVR25
9	Male	Black	37	Kidney	3	17 108	SOF/VEL ×12 weeks	0	Famotidine 20 mg BID​ Sodium bicarbonate 1300 mg BID​ Tacrolimus 17 mg daily​	+viral load 1 week post EOT	N/A	SOF/VEL/VOX ×12 weeks	2	Famotidine 20 mg BID​ Sodium bicarbonate 1300 mg BID​ Tacrolimus 12 mg daily​	+viral load 3 weeks post EOT e
10	Male	White	70	Kidney	3	28 080 785	GLE/PIB ×12 weeks	0	Famotidine 20 mg BID​ Pravastatin 20 mg daily​ Tacrolimus 9 mg daily​	+viral load 11 weeks post EOT	N/A	SOF/VEL/VOX ×12 weeks	0	Famotidine 20 mg daily​ Magnesium oxide 400 mg BID​ Pravastatin 20 mg daily​ Sodium bicarbonate 1300 mg BID​ Tacrolimus 5 mg daily​	Achieved SVR16
11	Male	White	57	Lung	1a	13 375 680	LDV/SOF ×12 weeks	0	Calcium carbonate 1250 mg daily​ Omeprazole 20 mg daily​ Magnesium oxide 400 mg daily​ Tacrolimus 4 mg BID​	+viral load 8 weeks post EOT	N/A	SOF/VEL/VOX ×24 weeks f	0	Calcium carbonate 1250 mg BID​ Omeprazole 20 mg daily for 45 days then changed to Famotidine 40 mg BID​ Tacrolimus 1 mg QAM and 0.5 mg QPM​ Warfarin 0.5 mg daily​	Achieved SVR27
12	Male	White	66	Heart	3	204 267	GLE/PIB ×12 weeks	0	Pantoprazole 40 mg daily​ Pravastatin 20 mg daily ​ Tacrolimus 4 mg BID​	+viral load at EOT	N/A	SOF/VEL/VOX ×12 weeks	0	Magnesium oxide 400 mg BID​ Pravastatin 40 mg daily​ Tacrolimus 2 mg BID​	Achieved SVR13
13	Female	White	31	Liver	1a	5 188 187	SOF/VEL ×12 weeks	0	Tacrolimus 3–5 mg BID​	+viral load 5 weeks post EOT	N/A	SOF/VEL/VOX + RBV ×12 weeks	0	Famotidine 20 mg daily​ Tacrolimus 3–5 mg BID​​	Achieved SVR75

Abbreviations: DAA, direct‐acting antiviral; DDI, drug/drug interaction; EOT, end of treatment; GLE/PIB, glecaprevir/pibrentasvir; GT, genotype; HCV, hepatitis C virus; LDV/SOF, ledipasvir/sofosbuvir; N/A, not available; NAT, nucleic acid test; RAS, resistance‐associated substitutions; RBV, ribavirin; SOF/VEL, sofosbuvir/velpatasvir; SOF/VEL/VOX, sofosbuvir/velpatasvir/voxilaprevir; SOT, solid organ transplant; SVR, sustained virologic response.

^a Baseline is defined as the most recent value prior to initiation of DAA.

^b GLE/PIB stopped early at discretion of the hepatology service due to rising viral load and emergence of RAS polymorphisms.

^c GLE/PIB stopped early at discretion of the hepatology service due to rising viral load.

^d Initially prescribed for 12 weeks; extended to 24 weeks at the discretion of the hepatology service due to persistent viremia and persistently elevated alanine transaminase (ALT).

^e Underwent third round of DAA treatment with sofosbuvir + GLE/PIB + RBV ×24 weeks. No RAS testing available. No reported missed doses. Achieved SVR14.

^f Initially prescribed for 12 weeks; extended to 24 weeks at the discretion of the hepatology service due to persistent viremia.

3.2. Initial DAA Treatment

Initial DAA regimens included sofosbuvir/velpatasvir (SOF/VEL) ×12 weeks (46%; 6/13), followed by glecaprevir/pibrentasvir (GLE/PIB) ×12 weeks (39%; 5/13) and ledipasvir/sofosbuvir (LDV/SOF) ×12 weeks (15%; 2/13). Median time from SOT to initial DAA treatment initiation was 35 days [IQR 22–41]. No patients reported missed doses during initial DAA treatment.

Figure 1 depicts the lab monitoring timeline in relation to DAA therapy. Four patients (IDs 5, 7, 9, and 12) never achieved an undetectable viral load during initial DAA treatment. DAA was discontinued early in two of these patients due to nonresponse; ID 5 at Week 11 and ID 7 at Week 10. Both demonstrated initial DAA response with HCV RNA decline by Week 4 (ID 5 = 12 IU/mL, ID 7 = 23 IU/mL), but by Week 8, HCV RNA increased (ID 5 = 19 542 IU/mL, ID 7 = 663 007 IU/mL). ID 9 and ID 12 initially responded to DAA with low levels of viremia (19 IU/mL and 60 IU/mL, respectively) at Week 4, but did not undergo repeat testing during treatment. ALT improved but did not normalize during initial treatment in two patients (IDs 2 and 8). ID 2's ALT improved from 184 to 80 U/L (Week 12) and ID 8's from 247 to 67 U/L (Week 8) while on treatment.

FIGURE 1.

DAA monitoring timelines. HCV RNA lab monitoring and ALT is depicted for each patient's DAA treatment. All patients except four (ID 5, ID 7, ID 9, and ID 12) achieved HCV RNA ≤ 15 IU/mL during initial DAA treatment. Two patients (ID 2 and ID 8) did not achieve normalization of ALT during initial DAA treatment. All patients except one (ID 10) achieved HCV RNA ≤ 15 IU/mL during subsequent DAA treatment. One patient (ID 9) required a third DAA treatment and did achieve HCV RNA ≤ 15 IU/mL during this time.

Potential DDIs were managed accordingly with the exception of two patients. ID 3 reported taking famotidine 4 h after SOF/VEL for the first 7 days of treatment despite instruction to take simultaneously due to potential decreased velpatasvir concentrations. Famotidine was discontinued following the first 7 days. ID 9 reported taking sodium bicarbonate simultaneously with SOF/VEL for the first 21 days of treatment despite instruction to separate 4 h from SOV/VEL due to potential decreased velpatasvir concentrations.

All 13 patients who completed therapy had a positive viral load by SVR12. IDs 6 and 12 were detectable at the end of treatment.

3.3. DAA Retreatment

The most common DAA retreatment regimen was sofosbuvir/velpatasvir/voxilaprevir (SOF/VEL/VOX) ×12 weeks (62%; 8/13) followed by SOF/VEL/VOX + ribavirin (RBV) ×12 weeks (15%; 2/13), GLE/PIB + RBV ×16 weeks (8%; 1/13), SOF/VEL/VOX + RBV ×24 weeks (8%; 1/13), and SOF/VEL/VOX ×24 weeks (8%; 1/13) (Table 1). Median time to retreatment following positive viral load was 35 days [IQR 17–76]. Three patients (IDs 1, 5, and 8) completed RAS testing following initial DAA treatment (Table 1). Three patients reported ≥ 1 missed dose during retreatment.

Two patients received a treatment extension from 12 to 24 weeks while on DAA. ID 8 did not achieve undetectable HCV RNA or normalized ALT after 12 weeks of treatment with SOF/VEL/VOX + RBV ×12 weeks (Figure 1). However, after extending treatment to 24 weeks and missing seven doses due to insurance delays, ALT normalized and HCV RNA became undetectable at week 21: ultimately achieving SVR25. ID 11's HCV RNA did not become undetectable until Week 11 of SOF/VEL/VOX ×12 but achieved SVR27 after treatment was extended to 24 weeks.

Potential DDIs were managed accordingly with the exception of two patients. ID 8 received rosuvastatin for 14 days concomitantly with SOF/VEL/VOX beginning Week 5 of DAA retreatment. This was subsequently changed to pravastatin. No statin‐related toxicities were noted. ID 9 reported taking famotidine 4 h after SOF/VEL/VOX for the first 21 days of treatment despite instruction to take simultaneously due to potential decreased velpatasvir concentrations.

One patient (ID 9) did not achieve SVR following DAA retreatment with SOF/VEL/VOX ×12 weeks, despite an undetectable HCV RNA on treatment at Week 11 and normal ALT at baseline. No RAS testing was completed. A third regimen, sofosbuvir (SOF) + GLE/PIB + RBV ×24 weeks, resulted in achievement of SVR14 with no identified potential DDIs.

4. Discussion

This multicenter case series provides real‐world insight into retreatment strategies and outcomes in HCV NAT+ D+/R− SOT recipients not achieving SVR following reactive DAA treatment. Varying initial DAA treatment strategies following HCV D+/R− SOTs exist throughout the literature regarding DAA regimen and timing of treatment initiation [11, 14, 19–22]. The American Association for the Study of Liver Diseases (AASLD) and Infectious Diseases Society of America (IDSA) recommend early, prophylactic/preemptive treatment when the patient is clinically stable [23]. Medication costs, formulary restrictions, and insurance barriers often limit this treatment strategy in the United States, including those presented herein, thusly, timing of treatment initiation is beyond this series' scope.

For reactive DAA treatment, the AASLD/IDSA recommends pangenotypic regimens GLE/PIB or SOF/VEL ×12 weeks, as genotyping is not always available in practice. In this series, all GTs were known and most patients treated with SOF/VEL or GLE/PIB ×12 weeks, aligning with current recommendations. Two patients initially received LDV/SOF ×12 weeks, however, these were GT 1 patients treated prior to inception of current AASLD/IDSA recommendations.

Interestingly, two HCV D+/R− kidney recipients (GT 1a and 2) receiving GLE/PIB ×12 weeks were nonresponders. Both transitioned to SOF/VEL/VOX ± RBV ×12 weeks, achieving SVR. Similar cases have been described in other real‐world reactive studies. First, a GT 1a kidney recipient with nonresponse after 4 weeks of GLE/PIB transitioned to SOF/VEL/VOX for an unknown duration. SVR was not available (N/A) at time of study publication [16]. The HCV‐TARGET study reported two nonresponders in their reactive‐treatment arm. Both were kidney recipients initially receiving GLE/PIB and SOF/VEL and both achieved SVR following SOF/VEL/VOX ×12 weeks [24]. In this series, nonresponse occurred most commonly in HCV D+/R− kidney recipients, however, despite nonresponse, SVR was achieved following retreatment with SOF/VEL/VOX ± RBV ×12 weeks.

Eleven patients in this series were considered relapsers, most commonly retreated with SOF/VEL/VOX ± RBV ×12–24 weeks. This strategy mirrors those employed in the literature. HCV‐TARGET reported three relapsers in their reactive arm including two lung recipients (GT 1a and GT 3) and one kidney recipient (GT unknown), all initially treated with SOF/VEL ×12 weeks. All achieved SVR following retreatment with SOF/VEL/VOX; both lung recipients received 24 weeks and the kidney recipient 12 weeks [24]. Other studies reporting successful DAA retreatment included three lung recipients; two reactively treated with SOF/VEL ×12 weeks, and one with GLE/PIB ×12 weeks who achieved SVR following SOV/VEL/VOX ± RBV ×24 weeks and SOF/VEL/VOX ×4 weeks, respectively [15, 25]. Similarly, a heart recipient reactively treated with an unknown duration of LDV/SOF and a kidney recipient reactively treated with LDV/SOF ×12 weeks achieved SVR following SOF/VEL/VOX for an unknown duration and 12 weeks, respectively [26, 27]. This series, as with existing literature, observed variability among donor organ type and retreatment strategies in DAA relapsers following HCV D+/R− SOT. Despite this, SVR was achieved following retreatment with SOF/VEL/VOX ± RBV ×12–24 weeks.

One GT 3 kidney recipient in this series underwent DAA retreatment twice to achieve SVR: SOF/VEL ×12 weeks and SOF/VEL/VOX ×12 weeks. Although limited to case studies in non‐transplant patients, general strategies employed in patients failing multiple DAAs included targeting multiple HCV proteins and extending treatment to 24 weeks [28, 29, 30]. Our patient achieved SVR with this strategy, employing SOF + GLE/PIB + RBV ×24 weeks.

All patients were treated reactively, medication regimens were stable and potentially significant DDIs were addressed prior to DAA selection. Four potential interactions were not initially managed per the University of Liverpool HEP Drug Interaction Checker but were appropriately addressed upon discovery [18]. The impact of these interactions on SVR is unknown, highlighting the importance of ongoing DDI assessment during DAA therapy, particularly given the frequency in which medications change in this population.

This case series, the largest and most comprehensive on DAA retreatment after initial failure in HCV D+/R− SOT, demonstrates high SVR rates. All patients achieved SVR following one or two retreatment courses, aligning with cases described in current literature. Despite its small size, this sampling is large given high DAA efficacy rates and thus enhances understanding of the HCV D+/R− SOT patients requiring DAA retreatment, subsequent retreatment strategies, and their efficacy.

Author Contributions

Alicia B. Carver: conceptualization, methodology, data curation, formal analysis, visualization, writing – original draft, validation. Claire Özoral: conceptualization, methodology, writing – review and editing, data curation. Morgan Lange: conceptualization, methodology, data curation, writing – review and editing. Alysa Mattise: conceptualization, methodology, data curation, writing – review and editing. Kristen Whelchel: methodology, writing – review and editing, visualization. Roman Perri: conceptualization, data curation, writing – review and editing. All authors approved the final manuscript.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Visual Abstract