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BA.3.2

From Wikipedia, the free encyclopedia
SARS-CoV-2 Variant
Omicron (BA.3.2)
Scientifically accurate atomic model of the external structure of SARS-CoV-2. Each "ball" is an atom.
Scientifically accurate atomic model of the external structure of SARS-CoV-2. Each "ball" is an atom.
General details
WHO DesignationOmicron (BA.3.2)
LineageB.1.1.529.3.2
First detectedSouth Africa
Date reported22 November 2024; 12 months ago (2024-11-22)
StatusVariant 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]
The genomic sequence of the BA.3.2 variant is pictured above

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]
Defining mutations in the
SARS-CoV-2 BA.3.2 variant
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]

References

[edit]
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