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: Introduction: New South Wales (NSW) has one of the world's highest uptake rates of HIV pre‐exposure prophylaxis (PrEP). This uptake has been credited with sharp declines in HIV transmission, particularly among Australian‐born gay and bisexual men. Concerns have been raised around the potential for the emergence of tenofovir (TFV) and XTC (lamivudine/emtricitabine) resistance in settings of high PrEP use. Such an emergence could also increase treatment failure and associated clinical outcomes among people living with HIV (PLHIV). Despite low levels of nucleoside reverse‐transcriptase inhibitor (NRTI) resistance relating to PrEP use in clinical settings, there are few published studies describing the prevalence of NRTI resistance among people newly diagnosed with HIV in a setting of high PrEP use. Methods: Using HIV antiretroviral drug resistance data linked to NSW HIV notifications records of people diagnosed from 1 January 2015 to 31 December 2021 and with HIV attributed to male‐to‐male sex, we described trends in TFV and XTC resistance. Resistance was identified using the Stanford HIV Drug Resistance genotypic resistance interpretation system. To focus on transmitted drug resistance, resistance prevalence estimates were generated using sequences taken less than 3 months post‐HIV diagnosis. These estimates were stratified by timing of sequencing relative to the date of diagnosis, year of sequencing, birthplace, likely place of HIV acquisition, and stage of HIV at diagnosis. Results: Among 1119 diagnoses linked to HIV genomes sequenced less than 3 months following diagnosis, overall XTC resistance prevalence was 1.3%. Between 2015 and 2021, XTC resistance fluctuated between 0.5% to 2.9% and was 1.0% in 2021. No TFV resistance was found over the study period in any of the sequences analysed. Higher XTC resistance prevalence was observed among people with newly acquired HIV (evidence of HIV acquisition in the 12 months prior to diagnosis; 2.9%, p = 0.008). Conclusions: In this Australian setting, TFV and XTC resistance prevalence in new HIV diagnoses remained low. Our findings offer further evidence for the safe scale‐up of PrEP in high‐income settings, without jeopardizing the treatment of those living with HIV., INTRODUCTION Australia has made remarkable progress in its effort to meet the UNAIDS 2030 target of ending AIDS as a public health threat with HIV diagnoses attributed to male‐to‐male sex [...]

Introduction: Due to a lack of robust population denominators, Australia is unable to accurately monitor changes in the HIV epidemic for some populations. The ratio of HIV transmission relative to the number of people with HIV (an incidence prevalence ratio, or IPR) can measure such changes. The IPR is measured against an IPR benchmark derived from post‐HIV acquisition life expectancy, to indicate whether an HIV epidemic is shrinking or growing. Using IPRs and Australia‐specific IPR benchmarks, this study aims to describe the Australian HIV epidemic among three groups: men with HIV attributed to male‐to‐male sex, women with HIV and people with HIV attributed to injection drug use. Methods: Using mathematical modelling derived from HIV notifications, cohort and administrative data, IPRs were generated for each of the three groups. These IPRs were compared with IPR benchmarks derived from post‐HIV acquisition mortality estimates using abridged life tables for men, women and people who inject drugs. The IPR benchmark for men was applied to people with HIV attributed to male‐to‐male sex. Trends in the IPR over time were described for each reported population from 2015 to 2022. Results: Overall, the IPR fell by 80%, from 0.040 (range: 0.034−0.045) in 2015 to 0.008 (range: 0.003−0.013) in 2022 and fell below the benchmark (0.022) in 2020. Among people with HIV attributed to male‐to‐male sex, the IPR fell by 85%, from 0.041 (range: 0.034−0.047) in 2015 to 0.006 (range: 0.003−0.024) in 2022 and fell below the benchmark (0.022) in 2020. Among women with HIV, the IPR fell by 56%, from 0.032 (range: 0.026−0.039) in 2015 to 0.014 (range: 0.003−0.029) in 2022 and fell below the benchmark (0.022) in 2019. Among people with HIV attributed to injection drug use, the IPR fell by 61%, from 0.036 (range: 0.022−0.047) in 2015 to 0.014 (range: 0.002−0.057) in 2022 and fell below the benchmark (0.028) in 2019. Conclusions: Australian IPRs in all populations examined have dropped below the level required to sustain the HIV epidemic at current levels. By applying this method in other contexts, the changing scale of HIV epidemics may be better described for populations lacking robust population denominators. [ABSTRACT FROM AUTHOR]

: Introduction: Australia has set the goal for the virtual elimination of HIV transmission by the end of 2022, yet accurate information is lacking on the level of HIV transmission occurring among residents. We developed a method for estimating the timing of HIV acquisition among migrants, relative to their arrival in Australia. We then applied this method to surveillance data from the Australian National HIV Registry with the aim of ascertaining the level of HIV transmission among migrants to Australia occurring before and after migration, and to inform appropriate local public health interventions. Methods: We developed an algorithm incorporating CD4[sup.+] T‐cell decline back‐projection and enhanced variables (clinical presentation, past HIV testing history and clinician estimate of the place of HIV acquisition) and compared it to a standard algorithm which uses CD4[sup.+] T‐cell back‐projection only. We applied both algorithms to all new HIV diagnoses among migrants to estimate whether HIV infection occurred before or after arrival in Australia. Results: Between 1 January 2016 and 31 December 2020, 1909 migrants were newly diagnosed with HIV in Australia, 85% were men, and the median age was 33 years. Using the enhanced algorithm, 932 (49%) were estimated to have acquired HIV after arrival in Australia, 629 (33%) before arrival (from overseas), 250 (13%) close to arrival and 98 (5%) were unable to be classified. Using the standard algorithm, 622 (33%) were estimated to have acquired HIV in Australia, 472 (25%) before arrival, 321 (17%) close to arrival and 494 (26%) were unable to be classified. Conclusions: Using our algorithm, close to half of migrants diagnosed with HIV were estimated to have acquired HIV after arrival in Australia, highlighting the need for tailored culturally appropriate testing and prevention programmes to limit HIV transmission and achieve elimination targets. Our method reduced the proportion of HIV cases unable to be classified and can be adopted in other countries with similar HIV surveillance protocols, to inform epidemiology and elimination efforts., INTRODUCTION UNAIDS has set the ambitious target to eliminate the global transmission of HIV by 2030 [1] and Australia is aiming for “virtual elimination” by the end of 2022 [2]. [...]

Introduction: The human immunodeficiency virus 1 (HIV-1) pandemic is characterized by numerous distinct sub-epidemics (clusters) that continually fuel local transmission. The aims of this study were to identify active growing clusters, to understand which factors most influence the transmission dynamics, how these vary between different subtypes and how this information might contribute to effective public health responses. Methods: We used HIV-1 genomic sequence data linked to demographic factors that accounted for approximately 70% of all new HIV-1 notifications in New South Wales (NSW). We assessed differences in transmission cluster dynamics between subtype B and circulating recombinant form 01AE (CRF01AE). Separate phylogenetic trees were estimated using 2919 subtype B and 473 CRF01AE sequences sampled between 2004 and 2018 in combination with global sequence data and NSW-specific clades were classified as clusters, pairs or singletons. Significant differences in demographics between subtypes were assessed with Chi-Square statistics. Results: We identified 104 subtype B and 11 CRF01AE growing clusters containing a maximum of 29 and 11 sequences for subtype B and CRF01AE respectively. We observed a > 2-fold increase in the number of NSW-specific CRF01AE clades over time. Subtype B clusters were associated with individuals reporting men who have sex with men (MSM) as their transmission risk factor, being born in Australia, and being diagnosed during the early stage of infection (p < 0.01). CRF01AE infections clusters were associated with infections among individuals diagnosed during the early stage of infection (p < 0.05) and CRF01AE singletons were more likely to be from infections among individuals reporting heterosexual transmission (p < 0.05). We found six subtype B clusters with an above-average growth rate (>1.5 sequences / 6-months) and which consisted of a majority of infections among MSM. We also found four active growing CRF01AE clusters containing only infections among MSM. Finally, we found 47 subtype B and seven CRF01AE clusters that contained a large gap in time (>1 year) between infections and may be indicative of intermediate transmissions via undiagnosed individuals. Conclusions: The large number of active and growing clusters among MSM are the driving force of the ongoing epidemic in NSW for subtype B and CRF01AE. Keywords: HIV1; transmission cluster; subtype B and CRF01AE; demographic differences; early infections; public health, 1 | INTRODUCTION Australia is at the forefront of successful control of human immunodeficiency virus type 1 (HIV-1) transmission due to rapid and comprehensive public health responses from the beginning [...]

: Introduction: The human immunodeficiency virus 1 (HIV‐1) pandemic is characterized by numerous distinct sub‐epidemics (clusters) that continually fuel local transmission. The aims of this study were to identify active growing clusters, to understand which factors most influence the transmission dynamics, how these vary between different subtypes and how this information might contribute to effective public health responses. Methods: We used HIV‐1 genomic sequence data linked to demographic factors that accounted for approximately 70% of all new HIV‐1 notifications in New South Wales (NSW). We assessed differences in transmission cluster dynamics between subtype B and circulating recombinant form 01_AE (CRF01_AE). Separate phylogenetic trees were estimated using 2919 subtype B and 473 CRF01_AE sequences sampled between 2004 and 2018 in combination with global sequence data and NSW‐specific clades were classified as clusters, pairs or singletons. Significant differences in demographics between subtypes were assessed with Chi‐Square statistics. Results: We identified 104 subtype B and 11 CRF01_AE growing clusters containing a maximum of 29 and 11 sequences for subtype B and CRF01_AE respectively. We observed a > 2‐fold increase in the number of NSW‐specific CRF01_AE clades over time. Subtype B clusters were associated with individuals reporting men who have sex with men (MSM) as their transmission risk factor, being born in Australia, and being diagnosed during the early stage of infection (p < 0.01). CRF01_AE infections clusters were associated with infections among individuals diagnosed during the early stage of infection (p < 0.05) and CRF01_AE singletons were more likely to be from infections among individuals reporting heterosexual transmission (p < 0.05). We found six subtype B clusters with an above‐average growth rate (>1.5 sequences / 6‐months) and which consisted of a majority of infections among MSM. We also found four active growing CRF01_AE clusters containing only infections among MSM. Finally, we found 47 subtype B and seven CRF01_AE clusters that contained a large gap in time (>1 year) between infections and may be indicative of intermediate transmissions via undiagnosed individuals. Conclusions: The large number of active and growing clusters among MSM are the driving force of the ongoing epidemic in NSW for subtype B and CRF01_AE., Introduction Australia is at the forefront of successful control of human immunodeficiency virus type 1 (HIV‐1) transmission due to rapid and comprehensive public health responses from the beginning of the [...]

Objectives: To understand the acquisition of resistance genes by a non-GC1, non-GC2 Acinetobacter baumannii strain responsible for a 4 year outbreak at a Sydney hospital.Methods: Representative isolates were screened for resistance to antibiotics. Three were subjected to WGS using Illumina HiSeq. One genome was completed with MinION long reads. Resistance regions were compared with known sequences using bioinformatics.Results: Isolates were resistant to third-generation cephalosporins, gentamicin and tobramycin, sulfamethoxazole and erythromycin. Sequenced isolates were ST49 (Institut Pasteur scheme) and ST128 (Oxford scheme) and carried KL11 at the capsule locus and OCL8 at the lipooligosaccharide outer core locus. The complete genome of isolate J9 revealed that the resistance genes were all in plasmids; pRAY* contained aadB, and a large plasmid, pJ9-3, contained sul2 and floR genes and a dif module containing the mph(E)-msr(E) macrolide resistance genes. Transposon Tn6168, consisting of a second copy of the chromosomal ampC gene region flanked by ISAba1s, confers resistance to third-generation cephalosporins. Tn6168 is located inside the mph(E)-msr(E) dif module. pJ9-3 includes a set of four dif modules and the orientation of the pdif sites, XerC-XerD or XerD-XerC, alternates. A large transposon, Tn6175, containing tniCABDE transposition genes and genes annotated as being involved in heavy metal metabolism, uptake or export was found in the comM gene. Other ST49:ST128:KL11:OCL8 genomes found in the GenBank WGS database carried Tn6175 but neither of the plasmids carrying the resistance genes.Conclusions: An early carbapenem-susceptible A. baumannii outbreak recorded in Australia was caused by an unusual clone that had acquired plasmids carrying antibiotic resistance genes. [ABSTRACT FROM AUTHOR]

The article offers presents a study related to the isolation of the AbGRI1 variant in an antibiotic-resistant bacteria, Acinetobacter baumannii belonging to global clone 2 (GC2). Topics discussed include information on the disc diffusion assay on K-16 strain reveals its resistance towards the ampicillin, ceftazidime and the cefotaxime; discussions on the use of the GenBank database for finding AbGRI1-5 as a unique gene; and the information on the AbGRI1-5 and AbGRI1-2 shares common ancestry.

Objectives: The objective of this study was to examine the evolution of carbapenem-resistant global clone 2 (GC2) Acinetobacter baumannii in Australia focusing on the complement of aminoglycoside resistance genes and their location in resistance islands and plasmids.Methods: Sixty-two carbapenem-resistant GC2 A. baumannii isolates with various aminoglycoside resistance profiles and resistance gene content that were recovered over the period 1999-2010 from hospitals on the east coast of Australia were examined. PCR was used to link relevant contigs retrieved from whole genomes sequenced using Illumina HiSeq and assembled de novo using Velvet. Resistance phenotypes were extended to include additional antibiotics using a disc diffusion assay.Results: Sixty-one isolates were ST208 (formerly ST92; Oxford scheme) and one was ST425. All isolates included the oxa23 carbapenem resistance gene in Tn2006 located in the same position in AbGRI1-2, along with the ISAba1-sul2-CR2Δ-tetA(B)-tetA(R)-CR2-strB-strA configuration. All isolates harboured either AbGRI2-1 carrying the aacC1 (gentamicin resistance) cassette or a variant derived from it via loss of some of the island content. When aacC1 was lost, aminoglycoside resistance was sometimes regained via acquisition of aadB (gentamicin, kanamycin and tobramycin resistance) in pRAY*-v1 or TnaphA6 (amikacin, kanamycin and neomycin resistance) in a repAci6 plasmid. A small cryptic plasmid or a deletion variant of this plasmid was always present and a large cryptic plasmid was also variably present.Conclusions: The extensively antibiotic-resistant GC2 isolates from Sydney, Brisbane and Canberra appear to have arisen from a single import that was introduced into Australia in, or prior to, 1999 that then evolved and spread. [ABSTRACT FROM AUTHOR]

Changes over time in HIV-1 subtype diversity within a population reflect changes in factors influencing the development of local epidemics. Here we report on the genetic diversity of 2364 reverse transcriptase sequences from people living with HIV-1 in New South Wales (NSW) notified between 2004 and 2018. These data represent >70% of all new HIV-1 notifications in the state over this period. Phylogenetic analysis was performed to identify subtype-specific transmission clusters. Subtype B and non-B infections differed across all demographics analysed (p < 0.001). We found a strong positive association for infections among females, individuals not born in Australia or reporting heterosexual transmission being of non-B origin. Further, we found an overall increase in non-B infections among men who have sex with men from 50 to 79% in the last 10 years. However, we also found differences between non-B subtypes; heterosexual transmission was positively associated with subtype C only. In addition, the majority of subtype B infections were associated with clusters, while the majority of non-B infections were singletons. However, we found seven non-B clusters (≥5 sequences) indicative of local ongoing transmission. In conclusion, we present how the HIV-1 epidemic has changed over time in NSW, becoming more heterogeneous with distinct subtype-specific demographic associations. [ABSTRACT FROM AUTHOR]

A320, isolated in the Netherlands in 1982 and also known as RUH134, is the earliest available multiply antibiotic-resistant (MAR) Acinetobacter baumannii isolate belonging to global clone 2 (GC2) and is the reference strain for this clone. The draft genome sequence of A320 was used to investigate the original location and configuration of the IS26-bounded AbGRI2 resistance island found in current GC2 isolates. PCR mapping and sequencing were used to order contigs composing the resistance islands. A320 contains two IS26-bounded resistance islands, AbGRI2-0a and AbGRI2-0b, of 7.8 kb and 25.4 kb, respectively. Together they contain blaTEM, aacC1, aadA1, sul1, catA1, and aphA1b genes, which confer resistance to antibiotics used clinically in the 1970s, as well as an incomplete mercury resistance module. Tracking the continuity of the chromosome and the target site duplications revealed that the two resistance islands were originally together as AbGRI2-0, an island of 32.4 kb, and were subsequently separated via an IS26-mediated intramolecular inversion that reversed the orientation of 1.54 Mb of the chromosome and duplicated an IS26. A320 contains an ancestral form of AbGRI2, and the original insertion site of the AbGRI2 island was identified. Many of the AbGRI2 versions present in the completed GC2 genomes can be derived from it via the variant AbGRI2-1. IS26-mediated inversions have also played a part in forming AbGRI2-0, and, upon reversal, large regions of AbGRI2-0 are identical to parts of AbaR0, the ancestral version of the AbaR islands present in GC1 isolates. This indicates a common source., (Copyright © 2016, American Society for Microbiology. All Rights Reserved.)