BA.3.2
| Omicron (BA.3.2) | |
| General details | |
|---|---|
| WHO Designation | Omicron (BA.3.2) |
| Lineage | B.1.1.529.3.2 |
| First detected | South Africa |
| Date reported | 22 November 2024 |
| Status | Variant under monitoring[1] |
| Symptoms | |
| Asymptomatic infection,[2] body ache,[2] cough,[2] fainting,[3] fatigue,[4] fever, headache,[5] loss of smell or taste,[6][7] — less common nasal congestion or running nose[5] night sweats,[8] — unique Omicron symptom, upper respiratory tract infection[9] skin rash,[10] sneezing,[5] sore throat[3] | |
| Major variants | |
BA.3.2 is a heavily mutated Omicron subvariant of SARS-CoV-2, the virus that causes COVID-19. The variant was descended from an ancestral version of Omicron Subvariant BA.3 that hadn't circulated since early 2022. BA.3.2 is notable for having more than 50 mutations on its spike protein relative to BA.3, and more than 70 spike mutations relative to the original Wuhan wildtype virus.[11][12] The subvariant, which was first detected in a sample from South Africa on 22 November 2024, was found by researchers to be concerning, due to the sheer number of its mutations. By November 2025, the variant was found to be circulating in multiple countries, including Australia, Germany, and the United States.[11][13] On 5 December 2025, the World Health Organization (WHO) declared BA.3.2 to be a variant under monitoring (VUM).[1]
Nomenclature
[edit]"BA.3.2" is a PANGO lineage ID number selected by scientists for the variant in question, based on its genetic lineage.[14] Ever since the emergence of the Omicron variant in late 2021, the World Health Organization (WHO) had stopped assigning new COVID variants Greek alphabet names, and in March 2023, they officially revised their policy to name only Variants of Concern (VOCs) – As no new COVID variants have been assigned the VOC status since the emergence of the parent Omicron lineage in Fall 2021, the WHO hasn't issued any new names since then.[15] The lack of new names from the WHO and the reliance on only PANGO lineage numbers to track new COVID variants led to frustration among scientists and other groups, with some scientists criticizing the post-Omicron naming policy as a public communication failure and creating a false sense of security,[16][17] and some in the media called the PANGO naming system "confusing" and even an "alphabet soup".[18][19] In late 2022, following the proliferation of numerous Omicron subvariants, a group of scientists proposed a new naming system for significant COVID variants, although this idea failed to gain traction.[17]
History
[edit]The BA.3.2 variant was first detected in South Africa around 22 November 2024,[1] although the variant didn't catch attention until March 2025, when it began spreading to other countries, such as Mozambique. The BA.3.2 variant was found to have at least 53 spike protein mutations compared to the ancestral BA.3 variant,[11][13] and over 70 spike mutations and 100+ mutations in general compared to the Wuhan wildtype virus.[12][20] South Africa was identified as the likely origin point of Omicron lineages BA.1, BA.2, BA.3, BA.4, BA.5, BA.2.86, and BA.2.87.1, with the Gauteng Province of South Africa playing a major role in the emergence and/or amplification of those major Omicron lineages.[21] While the viruses from the BA.2 lineage had completely dominated among circulating viruses since early 2022, this was the first time that a descendant of BA.3 had been spotted since the lineage had stopped circulating in early 2022,[11] leading some scientists to label BA.3.2 an "undead variant", and with some scientists believing that BA.3.2's stealthy, slow emergence could serve as a template for the emergence of future COVID variants.[22] Two sublineages, BA.3.2.1 and BA.3.2.2, were identified by 2025, each differing from the ancestral BA.3.2 by two spike mutations, with BA.3.2.1 having the H681R and P1162R spike mutations, and BA.3.2.2 having K356T and A575S. Of the two sublineages, the BA.3.2.2 subvariant was the dominant one, later having an especially pronounced growth around Perth, in Western Australia.[13] Notably, the ancestral BA.3.2 variant was never directly detected, and all genomic samples had originated from one of its two sublineages.[11] BA.3.2 was subsequently detected in Europe in April 2025, with The Netherlands reporting detections on April 2, and Germany reporting detections on April 29. The variant was later spotted in the United States and Australia, with the variant gaining significant ground in Australia.[13][11] Around 14 September 2025, the BA.3.2 variant comprised around 8% of wastewater samples from Perth, with the variant's share increasing to 20% by 21 September.[13] Researchers noted that BA.3.2 was potentially SARS-CoV-2's third major emergence event, with the last such occurrence being the emergence of the dominant BA.2.86 variant two years ago (particularly its primary sublineage, JN.1).[12][11]
On 29 September, the WHO Technical Advisory Group on COVID-19 Vaccine Composition (TAG-CO-VAC) identified BA.3.2 as a potentially-emerging variant, for consideration of the next year's COVID vaccine composition, designating the variant's spike antigens as antigens of interest for the December 2025 decision-making meeting, alongside the NB.1.8.1 and XFG subvariants from the JN.1 lineage.[23] In October 2025, GISAID stopped providing regular updates to its COVID-19 datasets in several of their databases, including Nextstrain, covSPECTRUM, and outbreak.info, severely limiting toolsets that had been used by the world to monitor and respond to emerging SARS-CoV-2 variants, and partially blinding variant hunters.[24] This came in the wake of numerous concerns that were raised about Peter Bogner's governance of GISAID.[25] On 5 December 2025, the WHO designated BA.3.2 as a variant under monitoring (VUM), citing the variant's many mutations and substantial antibody escape, and the variant's increasing growth in Western Australia. However, the WHO also believed that the variant did not yet demonstrate a sustained growth advantage over the other circulating SARS-CoV-2 variants (all of which were from the JN.1 lineage), nor increased rates of deaths and hospitalizations.[1] At that time, Western Australia was the epicenter of new BA.3.2 infections.[1]
Biology
[edit]Mutations
[edit]
| Part of a series on the |
| COVID-19 pandemic |
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The original Omicron Variant from late 2021 had over 53 mutations relative to the Wuhan-Hu-1 or B variant,[26][27] which was far more than any previous SARS-CoV-2 variant. Thirty-two of these pertained to the spike protein, which most vaccines target to neutralise the virus,[28] and 15 of those spike mutations were located in the Receptor Binding Domain (RBD), at residues 319–541.[29] At the time of its discovery, many of the mutations were novel and not found in previous SARS-CoV-2 variants.[30] The BA.3.2 variant had at least an additional 51 spike protein mutations compared to the ancestral BA.3 variant,[11][13] and it had over 70 spike mutations and 100+ mutations in general compared to the Wuhan wildtype virus.[12][20] A large majority of BA.3.2's spike protein mutations were in the Receptor Binding Domain (RBD) and the N-Terminal Domain (NTD). This was the most highly mutated variant identified since the emergence of the BA.2.86 variant two years earlier, which bore 90+ mutations itself, relative to the Wuhan wildtype.[31][32][33] BA.3.2 lacked the S:L455S spike mutation that was prominent in JN.1 (BA.2.86.1.1),[31] in addition to the N450D, F486P, and Y505H spike mutations; however, BA.3.2 also regained the G496S mutation that was present in Omicron BA.1; BA.3.2 also picked up the A435S mutation, which was one of the defining spike mutations of the JN.1 subvariant NB.1.8.1.[20][34] BA.3.2 was noted for having large-scale deletions in its ORF7 and ORF8 genes,[11] as well as significant deletions in the NTD region, specifically around the 1–306 residues, resulting in the variant having shorter NTD loops. The shortening of the NTD loops is know to dramatically increase spike cleavage and viral infectivity, in addition to increasing the spike instability.[35] Regions around the spike Furin-Cleavage Site (FCS) were also found to be completely rearranged in the BA.3.2 variant, and it also had the N679R and P681R mutations, which are known for increasing spike cleavage.[35] BA.3.2 was found to have a strong antibody evasion, which was attributed to point mutations in the variant's N1 and N5 loops, and a deletion in the N3 loop of the N-Terminal Domain (NTD), as well as the K356T (which created a new sequon), R403S, R408K, and R493Q mutations, which are known for being able to potentially alter the epitopes of Class 1/4 neutralizing antibodies.[13] BA.3.2's P681H spike mutation was located just before the polybasic sequence of the Furin-Cleavage Site (FCS), and was known for enhancing spike protein activation, viral entry, and cell-to-cell fusion, relative to the ancestral Wuhan wildtype virus. The Alpha and Theta variants, and most of the Omicron variant viruses had the P861H version of the mutation; the P681R version of the mutation was present in the Delta and Kappa variants.[20][1] BA.3.2 had two known sublineages, BA.3.2.1 and BA.3.2.2. The sublineages each differed from the ancestral BA.3.2 variant by two mutations each, with BA.3.2.1 having the H681R and P1162R spike mutations, and BA.3.2.2 having the K356T and A575S spike mutations.[13]
Immunity, contagiousness and virulence
[edit]| Gene | Amino acid |
|---|---|
| ORF1ab | nsp1: R24H |
| nsp1: Δ84-86 | |
| nsp1: R124C | |
| nsp1: A131V | |
| nsp1: S135R | |
| nsp1: Δ141-143 | |
| nsp2: G227S | |
| nsp2: A260T | |
| nsp2: A591V | |
| nsp2: K672N | |
| nsp2: A776V | |
| nsp3: T24I | |
| nsp3: G489S | |
| nsp3: G1307S | |
| nsp3: T1881I | |
| nsp3: V2071F | |
| nsp3: S2303F | |
| nsp4: T327I | |
| nsp4: T492I | |
| nsp4: T3090I | |
| nsp4: T3255I | |
| nsp5: P132H | |
| nsp5: K3353R | |
| nsp5: P3395H | |
| nsp6: Δ106-108 | |
| nsp6: A3657V | |
| nsp6: Δ3675-3677 | |
| nsp8: I3944L | |
| nsp12: R276C | |
| nsp12: P314L | |
| nsp12: P323L | |
| nsp12: I527T | |
| nsp13: R392C | |
| nsp14: I42V | |
| nsp14: I1566V | |
| nsp15: I112I | |
| Spike | P9L |
| R21T | |
| P26L | |
| A67V | |
| Δ69-70 | |
| T95I | |
| I101T | |
| Δ136-147 | |
| F157S | |
| N164K | |
| S172F | |
| Q183H | |
| K187T | |
| Δ210-211 | |
| L212I | |
| R214ins_ASDT | |
| V227L | |
| Δ242-243 | |
| H245N | |
| P251S | |
| G257V | |
| A264D | |
| I326V | |
| I332V | |
| G339Y | |
| A348P | |
| K356T | |
| S371F | |
| S373P | |
| S375F | |
| T376A | |
| R403K | |
| D405N | |
| R408S | |
| K417N | |
| A435S | |
| N440R | |
| V445A | |
| G446D | |
| L452W | |
| N460K | |
| S477N | |
| T478N | |
| E484K | |
| G496S | |
| Q498R | |
| N501Y | |
| Y529N | |
| E554D | |
| A575S | |
| E583D | |
| D614G | |
| H625R | |
| N641K | |
| V642G | |
| E654K | |
| H655Y | |
| Q677H | |
| N679R | |
| P681H | |
| A688D | |
| S704L | |
| N764K | |
| K795T | |
| D796Y | |
| A852K | |
| S939F | |
| Q954H | |
| N969K | |
| P1162L | |
| D1184E | |
| ORF3a | A103S |
| T223I | |
| E | T9I |
| T11A | |
| M | Q19E |
| A63T | |
| V66L | |
| ORF6 | D61H |
| ORF7b | F19L |
| ORF8 | Δ1-120 |
| I121L | |
| N | P13L |
| Δ31-33 | |
| R203K | |
| G204R | |
| Q241H | |
| S413R | |
| ORF9b | P10S |
| Δ27-29 | |
| Sources: Stanford University,[20] covSPECTRUM[36] | |
In mid-2022, Omicron subvariants BA.4 and BA.5 were found to be the most infectious versions of SARS-CoV-2 yet, with Omicron BA.2 having an estimated 1.4x increase in transmissibility over BA.1 (which had an , or Basic reproduction number, around 9.5 according to one estimate), and BA.4 and BA.5 estimated as having a further 1.4x increase in transmissibility, with some estimates for the variants' R0 being around 18.6, which would potentially make BA.4 and BA.5 more contagious than the Measles virus.[37] The XBB.1.5 subvariant, which attained dominance the following winter, had an estimated growth advantage 1.09–1.13 times greater than that of the BQ.1 and BQ.1.1 viruses from the previously dominant BA.5 lineage, based on data from North America and Europe.[38] By mid-2023, when the Omicron XBB lineage was dominant, some studies estimated that the R0 of the circulating Omicron subvariants had reached or even exceeded 20.[39] By the winter, the JN.1 lineage was found to have an Re (effective reproductive number) about 1.2 times greater than the previously dominant EG.5.1 (XBB.1.9.2.5.1) lineage, and 1.1 times greater than its parent BA.2.86 lineage, indicating a significantly increased transmissibility advantage over the earlier variants.[40] By comparison, studies in Fall 2025 found that the BA.3.2 variant had a strong immune evasion profile, with BA.3.2 being able to evade more antibodies than JN.1's NB.1.8.1 sublineage, and having a similar antibody evasion level to JN.1's XFG sublineage. Additionally, the BA.3.2.2 subvariant was found to be even more resistant to antibodies than BA.3.2.1. However, researchers also found that BA.3.2 viruses exhibited lower cell-cell fusogenicity and lower infectivity in pseudovirus assays, compared to JN.1 subvariants NB.1.8.1 and XFG, with BA.3.2 viruses also found to have lower ACE2 binding affinity than those JN.1 subvariants. Researchers believed that these drawbacks could hamper BA.3.2's ability to become more widespread globally, although they also noted the variant's potential to pick up more favorable mutations.[13][11] XFG was the dominant COVID variant at the time those studies were conducted.[41][42]
Signs and symptoms
[edit]Loss of taste and smell seem to be uncommon compared to other strains.[6][7] A unique reported symptom of the Omicron variant is night sweats,[8][43] particularly with the BA.5 subvariant.[44][45] A study performed between 1 and 7 December 2021 by the Centers for Disease Control found that: "The most commonly reported symptoms [were] cough, fatigue, and congestion or runny nose" making it difficult to distinguish from a less damaging variant or another virus.[46] Research published in London on 25 December 2021 suggested the most frequent symptoms stated by users of the Zoe Covid app were "a runny nose, headaches, fatigue, sneezing and sore throats."[5] A British Omicron case-control observational study until March 2022 showed a reduction in odds of long COVID with the Omicron variant versus the Delta variant of 0·24–0·5 depending on age and time since vaccination.[47]
See also
[edit]- Antigenic shift
- Original antigenic sin
- Saltation (biology)
- Timeline of the COVID-19 pandemic
- Timeline of the SARS-CoV-2 Omicron variant
- Variants of SARS-CoV-2
- Sikhulile Moyo, the scientist who discovered SARS-CoV-2 Omicron
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- ^ CDC COVID-19 Response Team (2021). "SARS-CoV-2 B.1.1.529 (Omicron) Variant — United States, December 1–8, 2021". MMWR. Morbidity and Mortality Weekly Report. 70 (50): 1731–1734. doi:10.15585/mmwr.mm7050e1. PMC 8675659. PMID 34914670.
{{cite journal}}: CS1 maint: numeric names: authors list (link) - ^ Antonelli, Michela; Pujol, Joan Capdevila; Spector, Tim D.; Ourselin, Sebastien; Steves, Claire J. (2022). "Risk of long COVID associated with delta versus omicron variants of SARS-CoV-2". The Lancet. 399 (10343): 2263–2264. Bibcode:2022Lanc..399.2263A. doi:10.1016/S0140-6736(22)00941-2. PMC 9212672. PMID 35717982.
External links
[edit]- Outbreak map with locations of the first 23 positive samples chronologically
- SARS-CoV-2 Variant PANGO Lineage IDs - GitHub
