Provirus Mutations of Human T-Lymphotropic Virus 1 and 2
(HTLV-1 and HTLV-2) in HIV-1-Coinfected Individuals
Karoline Rodrigues Campos,
a
Adele Caterino-de-Araujo
a
a
Laboratório de Pesquisa em HTLV, Centro de Imunologia, Instituto Adolfo Lutz, Coordenadoria de Controle de Doenças, Secretaria de Estado da Saúde, São Paulo, Brazil
Karoline Rodrigues Campos and Adele Caterino-de-Araujo contributed equally to this work. Author order was determined by order of increasing seniority.
ABSTRACT Provirus mutations of human T-lymphotropic virus 1 (HTLV-1), mostly
the lack of the 5= long terminal repeat (LTR) genomic region, have been described
and associated with severe adult T cell leukemia/lymphoma (ATLL), non-sense point
mutations with low proviral load, and Western blotting indeterminate results. Until
now, no information concerning provirus mutations of HTLV-2 and its consequences,
as well as those of HTLV-1/2 in HIV-coinfected individuals, had been described.
Therefore, we searched for these mutations in provirus samples of 44 HIV/HTLV-1-
and 25 HIV/HTLV-2-coinfected individuals. Using protocols well established for ampli-
fication and sequencing of segments of the LTR, env, and tax regions, we searched
for defective type 1 particles that retain LTRs and lack internal sequences and type 2
particles that lack the 5=LTR region. In addition, using as references the prototypes
ATK (HTLV-1) and Mo (HTLV-2), we searched for point mutations in the LTR and syn-
onyms and nonsynonymous mutations and non-sense mutations in env and tax re-
gions. Defective HTLV-1 and HTLV-2 provirus type 1 or 2 was detected in 31.8% of
HIV/HTLV-1- and 32.0% of HIV/HTLV-2-coinfected individuals. Synonymous and non-
synonymous mutations were identified mostly in HTLV-2 and associated with lower
levels of specific antibodies. No non-sense mutations that resulted in premature ter-
mination of Env and Tax proteins were detected. On the contrary, mutation in the
stop codon of Tax2a produced a long protein characteristic of the HTLV-2c subtype.
The clinical significance of these mutations in coinfected individuals remains to be
defined, but they confirmed the lower sensitivity of serological and molecular diag-
nostic tests in HIV/HTLV-1/2 coinfections.
IMPORTANCE HTLV-1 and HTLV-2 are endemic to Brazil, and they have different ef-
fects in HIV/AIDS disease progression. HIV/HTLV-1 has been described as accelerating
the progression to AIDS and death, while HIV/HTLV-2 slows the progression to AIDS.
Provirus mutations of HTLV-1 were implicated in severe leukemia development and
in problems in the diagnosis of HTLV-1; in contrast, provirus mutations of HTLV-2
had not been confirmed and associated with problems in HTLV-2 diagnosis or dis-
ease outcome. Nevertheless, data obtained here allowed us to recognize and under-
stand the false-negative results in serologic and molecular tests applied for HTLV-1
and HTLV-2 diagnosis. Defective proviruses, as well as synonymous and nonsynony-
mous mutations, were associated with the diagnosis deficiencies. Additionally, since
HIV-1 and HTLV-1 infect the same cells (CD4 positive), the production of HIV-1 pseu-
dotypes with HTLV-1 envelope glycoprotein during HIV/HTLV-1 coinfection cannot
be excluded. Defective provirus of HTLV-2 and Tax2c is speculated to influence pro-
gression to AIDS.
KEYWORDS human T-lymphotropic virus 1, HTLV-1, human T-lymphotropic virus 2,
HTLV-2, HIV, coinfection, provirus mutation, sequencing, diagnostic impairment
Citation Campos KR, Caterino-de-Araujo A.
2020. Provirus mutations of human T-
lymphotropic virus 1 and 2 (HTLV-1 and HTLV-
2) in HIV-1-coinfected individuals. mSphere
5:e00923-20. https://doi.org/10.1128/mSphere
.00923-20.
Editor Akira Ono, University of Michigan
Medical School
Copyright © 2020 Campos and Caterino-de-
Araujo. This is an open-access article
distributed under the terms of the Creative
Commons Attribution 4.0 International license.
Address correspondence to Adele Caterino-de-
Araujo, adele.caterino@ial.sp.gov.br.
Received 10 September 2020
Accepted 13 September 2020
Published
RESEARCH ARTICLE
Molecular Biology and Physiology
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