Executive Summary
PQ.16.1.1, an NB.1.8.1-descendent SARS-CoV-2 lineage, has been designated a variant under monitoring (VUM) with increasing proportions globally, driven largely by detections in the Western Pacific Region, particularly Singapore.
Considering the available evidence, the additional public health risk posed by PQ.16.1.1 is evaluated as low at the global level.
Its mutation profile may confer additional immune escape, although direct phenotypic evidence is currently limited.
Available surveillance does not indicate increased clinical severity compared with other circulating variants, and existing vaccines are expected to continue providing protection against severe disease.
Initial Risk Evaluation of PQ.16.1.1, 27 July 2026
PQ.16.1.1 is a descendant of the Omicron JN.1-derived lineage NB.1.8.1, with the earliest available sequence collected on 25 March 2026.
Compared with NB.1.8.1, PQ.16.1.1 has the additional Spike substitutions D253G, N417T, D420N and I478T, together with Nucleocapsid T135I and ORF8 G8E [1].
PQ.16.1.1 is one of seven VUMs tracked by the WHO and was designated as a VUM on 27 July 2026.
The parent lineage NB.1.8.1 has demonstrated robust soluble human ACE2 engagement and pseudovirus infectivity, with only marginal additional immune evasion compared with LP.8.1 [2,3].
Preliminary PQ.16.1.1-specific data indicate that its receptor-binding domain binds human ACE2 with significantly lower affinity than that of NB.1.8.1 (KD: 16.5 nM versus 8.22 nM).
Consistent with this, soluble human ACE2 showed reduced neutralization of PQ.16.1.1 pseudoviruses compared to NB.1.8.1 (IC50: 0.22 µg/mL versus 0.17 µg/mL).
Neutralizing antibody titres against PQ.16.1.1 and NB.1.8.1 were broadly similar in plasma from individuals with prior Omicron exposure.
In plasma from Wuhan-Hu-1-primed individuals, titres against PQ.16.1.1 were modestly lower than those against NB.1.8.1.
PQ.16.1.1 also showed substantially reduced susceptibility to class 1 RBD-targeting monoclonal antibodies.
These preliminary findings suggest that the growth of PQ.16.1.1 is unlikely to be explained by enhanced ACE2 receptor binding alone and may instead be partly related to escape from specific antibody classes [4].
As of 8 July 2026, 457 PQ.16.1.1 sequences with collection dates through epidemiological week (EW) 25 had been submitted to GISAID from eight countries [1].
Of these, 438 (95.8%) were from the Western Pacific Region (WPR), including 388 (84.9% of the global total) from Singapore.
The remaining sequences were reported from Hong Kong SAR (34), Australia (10), the United States of America (10), Canada (8), the Republic of Korea (5), France (1) and Taiwan, China (1).
No PQ.16.1.1 have been reported from the African (AFR) and Eastern Mediterranean (EMR) Regions.
Globally, the proportion of PQ.16.1.1 among available sequences increased from 2.7% in EW 18 to 29.6% in EW 25, Table 1.
Over the same period, its proportion increased from 5.4% to 39.3% in WPR. In the Region of the Americas, PQ.16.1.1 represented 6.4% of available sequences in EW 25, although this estimate was based on only three of 47 sequences.
Singapore reported an increase from 12.6% in EW 18 to 55.1% in EW 25. In Hong Kong SAR, the proportion increased from 20.0% to 66.7%, with fluctuations, but the EW 25 estimate was based on four of six sequences submitted that week. In Singapore, sentinel SARS-CoV-2 test positivity increased rapidly from 6.5% in EW 16 to a peak of 19.8% in EW 19. Test positivity remained elevated through EW 22 before declining through EW 25.
The timing and magnitude of the increase were consistent with the seasonal pattern observed in 2024 and 2025.
Compared with 2025, however, the period of elevated test positivity was shorter, with a more rapid decline following the peak.
No case or death data were reported to WHO during the reporting period [5].
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WHO and its Technical Advisory Group on Virus Evolution (TAG-VE) continue to recommend that Member States prioritize specific actions to address the remaining uncertainties concerning PQ.16.1.1:
• Confirm the preliminary neutralization findings using live-virus and pseudovirus assays with contemporary human sera representative of affected populations and varied vaccination and infection histories.
• Undertake comparative studies of cell entry, replication, fusogenicity and Spike processing in the complete PQ.16.1.1 genetic background.
• Conduct comparative evaluations of hospitalization, intensive-care admission and death, controlling for age, prior immunity, comorbidities and time since vaccination or infection.
• Assess the performance of antigen-based and molecular diagnostic assays and determine phenotypic susceptibility to available direct-acting antivirals.
WHO and its Technical Advisory Group on COVID-19 Vaccine Composition (TAG-CO-VAC) continue to assess the impact of SARS-CoV-2 evolution on the performance of COVID-19 vaccines.
In its May 2026 recommendation, WHO TAG-CO-VAC advised the use of monovalent LP.8.1 as a COVID-19 vaccine antigen, while noting that other antigens, including XFG or NB.1.8.1, could also be used if they demonstrate broad and robust neutralizing-antibody responses or effectiveness against circulating variants.
Vaccination should not be delayed in anticipation of access to vaccines containing an updated antigen, and populations at highest risk of severe disease remain the priority [6].
No PQ.16.1.1-specific vaccine-effectiveness estimates are currently available.
The risk evaluation below follows the published WHO framework for risk evaluation of SARS-CoV-2 variants [7] and is based on evidence available as of 21 July 2026.
This risk evaluation should be revised as additional epidemiological, phenotypic and clinical evidence becomes available.
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References
{1} Khare, S.; Gurry, C.; Freitas, L.; Schultz, M.B.; Bach, G.; Diallo, A.; Akite, N.; Ho, J.; Lee, R.T.C.; Yeo, W.; et al. GISAID’s Role in Pandemic Response. China CDC Wkly. 2021, 3, 1049–1051, doi:10.46234/ccdcw2021.255.
{2} Guo, C.; Yu, Y.; Liu, J.; Jian, F.; Yang, S.; Song, W.; Yu, L.; Shao, F.; Cao, Y. Antigenic and Virological Characteris cs of SARS-CoV-2 Variants BA.3.2, XFG, and NB.1.8.1. Lancet Infect. Dis. 2025, doi:10.1016/S1473-3099(25)00308-1.
{3} WHO World Health Organiza on Technical Advisory Group on COVID-19 Vaccine Composition: Statement on the Antigenic Compositon of COVID-19 Vaccines 15 May 2025.
{4} He, P.; Song, Y.; Guo, C.; Yu, L.; Yu, Y.; Jian, F.; Shao, F.; Cao, Y. Antibody Evasion and Receptor Binding of SARS-CoV-2 Variants PQ.16.1.1 and RK.1. 2026, doi:10.64898/2026.07.21.739818.
{5} World Health Organiza on WHO COVID-19 Dashboard 2026.
{6} WHO World Health Organiza on Technical Advisory Group on COVID-19 Vaccine Composition: Statement on the Antigen Composition of COVID-19 Vaccines 16 May 2026.
{7} World Health Organiza on SARS-CoV-2 Variant Risk Evaluation, 30 August 2023; World Health Organization: Geneva, 2023;
{8} Planas, D.; Staropoli, I.; Michel, V.; Lemoine, F.; Dona , F.; Prot, M.;Porrot, F.; Guivel-Benhassine, F.; Jeyarajah, B.; Brisebarre, A.; et al. Distinct Evolution of SARS-CoV-2 Omicron XBB and BA.2.86/JN.1 Lineages Combining Increased Fitness and An body Evasion. Nat. Commun. 2024, 15, 2254, doi:10.1038/s41467-02446490-7. 6
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