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1102A AASLD ABSTRACTS HEPATOLOGY, October, 2015<br />

ratio for models including behavioural risk heterogeneity. Conclusions:<br />

Preferential mixing by HIV status and behavioural risk<br />

heterogeneity could be the main factors that have resulted in<br />

much higher HCV prevalence amongst HIV-positive MSM than<br />

in HIV-negative MSM. Greater HCV transmission could occur<br />

amongst HIV-negative MSM if HIV-negative MSM start using<br />

condoms less or mix more with HIV-positive MSM, something<br />

that may occur with widespread use of HIV pre-exposure prophylaxis.<br />

The effects of new HIV prevention interventions on<br />

HCV transmission should be considered.<br />

Disclosures:<br />

The following authors have nothing to disclose: Louis W. MacGregor, Peter Vickerman,<br />

Natasha K. Martin, Ford Hickson, Peter Weatherburn<br />

1831<br />

Positive Impact of Point of Care Testing and an Informational<br />

Brochure on Screening of the HCV Birth Cohort in<br />

a Rural New England Tertiary Care Center<br />

Arvind Suguness 1 , Casey M. Kolb Nava 1 , Kristen Ray 2 , Rolland C.<br />

Dickson 2 ; 1 Internal Medicine, Dartmouth Hitchcock Medical Center,<br />

White River Junction, VT; 2 Gastroenterology and Hepatology,<br />

Dartmouth Hitchcock Medical Center, Lebanon, NH<br />

Background. Hepatitis C Virus (HCV) screening of the Birth<br />

Cohort (BC) has been recommended by the CDC and USPSTF<br />

due to the high prevalence of HCV and advanced liver disease<br />

in this population. The use of risk-based screening was<br />

previously shown to be ineffective at identifying patients with<br />

HCV infection. To address these guidelines, we implemented<br />

a point-of-care testing (POCT) strategy for HCV, and surveyed<br />

patients within the cohort. The aim of this study was to assess<br />

factors in a HCV testing algorithm that influenced screening.<br />

Methods. A HCV BC screening initiative was fully implemented<br />

in an Internal Medicine Residents Clinic in a rural tertiary care<br />

center in the NE United States on 4-1-2014. BC patients (1945-<br />

1965) were identified by a prompt in the electronic medical<br />

record prior to arrival to clinic. They were given a brochure on<br />

HCV natural history, POCT, and HCV treatment at the time of<br />

check in. When patients were roomed they were offered testing<br />

with the Orasure finger prick test. The patients were given a<br />

questionnaire while they waited for the provider. HCV screening<br />

(+ or -) results were available within 20 minutes during the<br />

provider visit. Patients were informed of the results and those<br />

with positive results were offered same day PCR testing, with<br />

genotype performed if viral load was present. Results. There<br />

were 325 total respondents to the survey. Sixty three (19.4%)<br />

reported being asked by a health care provider to be tested<br />

for HCV in the past. Twenty one reported prior HCV testing<br />

(6.5%) and 8 reported a prior positive test (2.5%). Of the total<br />

respondents, 86 (26%) opted out of screening entirely, while<br />

239 patients (73.5%) chose to be screened at that visit. Of<br />

those screened, 117 (49.0%) said the information in the brochure<br />

or having test results immediately available influenced<br />

their decision to be tested. At least one reported risk factor<br />

was present in 142 patients (43.69%). Patients with at least<br />

one risk factor were no more likely to desire screening than<br />

those without risk factors (73.2% vs 73.8%, p=0.914). Patients<br />

with risk factors were no more likely than those without risk<br />

factors to report that the brochure or the immediately available<br />

results influenced their decision to get tested (43.2% vs 53.3%,<br />

p=0.123). Summary and Conclusion. Prior to initiation of a<br />

POCT strategy, relatively few patients in the birth cohort at<br />

our institution had been approached by health care providers<br />

about HCV screening and fewer still had been tested. The presence<br />

of an informational brochure, combined with point-of-care<br />

testing, significantly increased the number of patients with and<br />

without risk factors to undergo testing.<br />

Disclosures:<br />

Casey M. Kolb Nava - Consulting: AbbVie<br />

Kristen Ray - Advisory Committees or Review Panels: Abbvie<br />

Rolland C. Dickson - Advisory Committees or Review Panels: Biotest; Speaking<br />

and Teaching: gilead<br />

The following authors have nothing to disclose: Arvind Suguness<br />

1832<br />

Stability and prevalence of the NS3 Q80K polymorphism<br />

over time within HCV genotype 1a infected<br />

patients in Canada<br />

Jeffrey B. Joy 1 , Weiyan B. Dong 1 , Celia B. Chui 1 , Chanson J.<br />

Brumme 1 , Art Poon 1,3 , Huong Hew 2 , Richard Harrigan 1,3 ; 1 BC<br />

Centre for Excellence in HIV/AIDS, Vancouver, BC, Canada;<br />

2 Clinical Affairs, Janssen Incorporated, North York, ON, Canada;<br />

3 Medicine, University of British Columbia, Vancouver, BC, Canada<br />

Background: HCV genotype 1a (GT1a) infections harbouring a<br />

baseline Q80K polymorphism in the NS3 gene display reduced<br />

virologic response to IFN-based HCV treatments containing<br />

simeprevir. The prevalence of this and other NS3 resistance<br />

mutations in Canadian populations is not well described. Further,<br />

in the context of individual infections, the stability of this<br />

polymorphism among untreated patients over time is unknown.<br />

Methods: Using plasma samples serially collected over a<br />

10-year period from 121 HCV treatment naïve GT1a infected<br />

seroconverting injection drug users, we sought to investigate<br />

gain or loss of the Q80K polymorphism over time. A 1200-<br />

or 564-bp HCV NS3 fragment was sequenced by Sanger<br />

methods. Each sample was HLA typed to confirm database<br />

annotations on source individuals. HCV sequences were multiply<br />

aligned using MAFFT v7.154b. Phylogenetic trees were<br />

inferred using an approximate maximum likelihood method<br />

(FastTree2) and rooted under a molecular clock model using<br />

Path-O-Gen. To establish the prevalence of Q80K in Canadian<br />

Provinces, samples from GT1 LiPA HCV+ individuals were<br />

examined. Sequences were also screened for mutations associated<br />

with boceprevir/telaprevir resistance. Results: No patients<br />

whose first and last samples formed a monophyletic group<br />

altered their Q80K status. Nine patients changed genotypes<br />

(6 GT3a to GT1a, 2 GT1a to GT3a, and 1 GT1b to GT1a).<br />

Furthermore, in 10 patients, GT1a infections did not form a<br />

monophyletic group. Both between genotype and within genotype<br />

changes in viral lineage between collection dates suggest<br />

either (1) clearance followed by reinfection with a new variant<br />

or (2) a mixed infection. In sum, we observed 9 changes in<br />

Q80K in 121 patients, but in every case this resulted from<br />

patients switching HCV lineages rather than a mutation in<br />

their original HCV lineage. Prevalence of Q80K in Canada<br />

was 956/1835 (52%) in GT1a and provinces displayed no<br />

significant difference in prevalence of Q80K. Mutations associated<br />

with boceprevir or telaprevir resistance in this newly<br />

diagnosed population were also observed. Conclusions: These<br />

results suggest that, in the absence of therapy, Q80K is highly<br />

stable within HCV lineages and does not evolve in response<br />

to immune or other host specific effects. Observed changes<br />

in infection status amongst these patients supports genotypic<br />

and resistance testing of patients prior to starting IFN-based<br />

therapy, particularly amongst those at high risk of exposure to<br />

new variants of HCV such as intravenous drug users.<br />

Disclosures:<br />

Huong Hew - Employment: Janssen<br />

Richard Harrigan - Consulting: ViiV Health Care, Tobira Therapeutics, Selah<br />

Genomics Inc, Quest Diagnostics; Stock Shareholder: Merck, Gilead

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