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Infectious Disease and Neurocognition
aect whether HAM/ TSP occurs (Saito, 2019). HAM/ TSP is not the only neurological disease that has been associated with HTLV- 1. Other neurological diseases that
have been associated with HAM/ TSP include HTLV- 1- associated polymyositis,
HTLV- 1- associated polyneuropathy, diuse encephalomyelopathy, amyotrophic
lateral sclerosis- like syndrome associated with HTLV- 1, and HTLV- 1- associated
dysautonomia. HTLV- 1- associated dysautonomia might always occur in the context
of HAM/ TSP (Araujo, 2015). As a group, these HTLV- 1- associated diseases indicate
that HTLV- 1 may aect a variety of neurological functions.
Cognitive dysfunction associated with HTLV- 1
Quality of life is impaired in both asymptomatic carriers of HTLV- 1 and even
more so in HTLV- 1 patients with HAM/ TSP, with 12 percent of people in a
sample from both the United Kingdom and Brazil reporting a poor quality of
life (Rosadas et al., 2020), suggesting that even seemingly asymptomatic HTLV- 1
can aect well- being. Further, while cognitive decits have been associated with
spinal cord injury (Craig et al., 2017) such as occurs with HAM/ TSP, cognitive
dysfunction has also been associated with HTLV- 1 seropositivity in both patients
with HAM/ TSP and in otherwise asymptomatic carriers of HTLV- 1 (Gascón
et al., 2017) and may be part of the neurological decits associated with HTLV- 1
(Silva et al., 2003).
An animal model of HTLV- 1 infection showed adverse eects on working and
fear memory (Moghadam et al., 2018). In some cases, early cognitive impairment
in humans could occur before evidence of overt HAM/ TSP. Rosa de Castro (2020)
describe a 51- year- old man seropositive for HTLV- 1 but without evidence of spinal
cord involvement who presented with decits in auditory comprehension and executive memory. e initial evaluation showed an abnormal P300 event- related
potential, abnormal central auditory processing, and abnormal galvanic vestibular evoked myogenic potential but with a normal neurological examination and
normal cognitive screening. Two years later, though, the patient’s P300 and galvanic vestibular evoked myogenic potential had worsened, and he had developed a
Babinski sign. He also had developed mild cognitive impairment. In this case, there
was evidence that the patient’s cortical involvement had developed before overt
spinal cord disease.
HAM/ TSP is also associated with cognitive impairment. In a study comparing
patients having HAM/ TSP for a mean time of 17.8 years with healthy controls, the
HAM/ TSP patients had worse global cognitive function and worse executive function. In the HAM/ TSP group, the cognitive dysfunction was associated with decreased immunoglobulin M and increased immunoglobulin G, tumor necrosis
factor alpha, and interleukin 6, leading the authors of this study to speculate that
inammation associated with the HAM/ TSP could be involved with cognitive dysfunction in patients with HAM/ TSP (Champs et al., 2019).
Human T-Cell Lymphotropic Virus Type 1 89
While no dierences in performance on cognitive screening tests were found
between healthy controls, asymptomatic carriers of HTLV- 1 in another study (de
Paula et al., 2021), symptomatic carriers but without HAM/ STP, and patients with
HAM/ TSP, all the HTLV- 1 groups including the asymptomatic HTLV- 1 carriers had
worse cognitive function with additional neuropsychological testing compared to
the healthy controls. In summing up their ndings in the abstract of this paper, the
authors wrote, “HTLV- 1 is never a benign condition” (de Paula et al., 2021, p. 849),
highlighting the ndings that even otherwise asymptomatic HTLV- 1 carriers had
some decits in cognitive function. Cognitive impairment was present in an HTLV1 sample from Brazil of which 36 percent had HAM/ STP, although cognitive impairment was found even in patients without HAM/ STP, leading the authors of the study
to conclude that cognitive impairment is a part of HTLV- 1 infection (Goncalves
et al., 2017).
Silva et al. (2003) found mild cognitive impairment including decits in verbal
and visual memory, verbal uency, psychomotor speed, and selective and alternate
attention in both patients with HAM/ TSP and otherwise asymptomatic carriers of
HTLV- 1 compared to controls. In addition, cognitive dysfunction did not dier between both the HAM/ TSP and the asymptomatic carrier groups. A study from Brazil
comparing cognitive function between patients with HAM/ TSP, asymptomatic carriers of HTLV- 1, and non- infected controls found that the patients with HTLV- 1
as a group had some amount of cognitive dysfunction compared to 30 percent of
the healthy control group. Major neurocognitive disorder was found only in the
HAM/ TSP group, whereas all the asymptomatic carriers had mild neurocognitive
impairment. Decreased function in uid intelligence, intellectual function, visual
memory, and processing speed compared to the healthy control group characterized
the HTLV- 1- positive group (Gascón et al., 2017). Despite the evidence indicating
that HTLV- 1 infection both in patients with HAM/ TSP and in asymptomatic carriers is associated with worse cognitive function, Erickson et al. (2021) found no
associations between HTLV- 1 and cognitive function in a sample from the United
Kingdom. e dierences in cognitive outcome associated with HTLV- 1 between
this sample and other samples primarily from Brazil suggest that other demographic
and socioeconomic factors including overall exposure to other infectious disease
could moderate associations between HTLV- 1 and cognitive outcome. Indeed, socioeconomic factors and early- life adversity possibly inuence outcomes of other
infectious diseases such as inuenza and Covid- 19 (Holuka et al., 2020), suggesting
that similar factors could inuence associations between HTLV- 1 and cognitive
function. Holuka et al. (2020) argue that early- life adversity can have long- lasting effect on immune function including increasing its proinammatory eects. As such,
early- life adversity and socioeconomic factors could be among the factors determining how HTLV- 1 infection can aect neuropsychiatric and cognitive outcomes
and could be important variables in explaining dierences between studies that have
evaluated associations between HTLV- 1 infection and cognitive and neuropsychiatric function.
Infectious Disease and Neurocognition
Association between HTLV- 1 and dementia
An early study examining the association between HTLV- 1 and dementia in patients
and healthy controls aged 50– 89 years from areas in Japan endemic for HTLV- 1 that
excluded patients with HAM/ TSP found an association between HTLV- 1 and vascular dementia but not Alzheimer’s disease (Kira et al., 1997).
HTLV- 1 and depression and anxiety
In addition to its associations with neurological diseases, cognitive dysfunction,
and possibly dementia, HTLV- 1 also has been associated with depression and anxiety in both animal models and in humans. Moghadam et al. (2018) found that
HTLV- 1- infected mice had behavior suggestive of depression, consistent with some
ndings in humans (Rocha- Filho & Goncalves, 2018).
In humans, controversy exists as to whether HTLV- 1 is associated with depression
and anxiety. An early, cross- sectional study from Brazil based on 50 patients with
HTLV- 1 found that 42 percent had some type of a mental disorder, with 34 percent
having a mood disorder, most commonly depression, and 22 percent having some
type of an anxiety disorder, most commonly generalized anxiety disorder. e prevalence of mental disorder in the symptomatic patients was numerically higher than
in the HTLV- 1 asymptomatic patients, but the dierence did not reach statistical
signicance. e lack of a control group in this study limited comparison with the
HTLV- 1 seronegative population in this region of Brazil (de Carvalho et al., 2009).
In a sample from the United States of former blood donors, there were no associations between HTLV- 1 and major depression and generalized anxiety disorder in
statistical models adjusted for demographic and overall health variables (Guiltinan
et al., 2013). Although not nding an overall association with HAM/ TSP compared
to HTLV- 1 patients without HAM/ TSP, one study found that age may aect the relationship between HAM/ TSP and depression, with HAM/ TSP patients aged 18–
39 years having a higher prevalence of depressive symptoms (Boa- Sorte et al., 2015).
e results of a cross- sectional study from Brazil comparing depression and anxiety
as determined by a rating scale in patients seropositive for HTLV- 1 who also had
spastic paresis, asymptomatic patients seropositive for HTLV- 1, and control patients
seronegative for HTLV- 1 who were seen in a family practice clinic showed statistically signicant elevations of depression and anxiety in both HTLV- 1 groups compared to the control group (Rocha- Filho & Goncalves, 2018). In a sample from Brazil
that included HTLV- 1 seropositive patients with and without HAM/ TSP, 66 percent
of patients had anxiety and 64 percent had depression (Goncalves et al., 2017). An
earlier study comparing the prevalence of depression in asymptomatic patients seropositive for HTLV- 1 to seronegative controls found that HTLV- 1 seropositivity
was associated with depression, although not all HTLV- 1 seropositive patients had
Human T-Cell Lymphotropic Virus Type 1 91
evidence of depression (Stumpf et al., 2008). In another study from Brazil, patients
with HAM/ TSP had more depression and anxiety than did asymptomatic HTLV- 1
carriers (Gascón et al., 2011), although it is unclear whether the increased depression
and anxiety in this study resulted from additional factors associated with HAM/ TSP
itself or the psychosocial burden from the neurological impairments of HAM/ TSP.
A meta- analysis found that 35 percent of people with HTLV- 1 had clinically significant symptoms of depression or a diagnosis of depression and that 33 percent had
clinically signicant symptoms of anxiety or a diagnosis of anxiety. Furthermore,
the odds of having depression or anxiety were higher in patients with HTLV- 1 than
in controls without HTLV- 1 (Souza et al., 2021). In addition to noting that more research into associations between asymptomatic carriers of HTLV- 1 and depression
is needed, Souza et al. (2021) also write that it is important to evaluate associations
between HTLV- 1 and anxiety and depression from regions outside of Brazil as socioeconomic conditions can vary across dierent regions, factors that might modify
the relationship between HTLV- 1 and anxiety and depression. In this regard, a study
based on data from the UK Biobank found no associations between either HTLV- 1
seropositivity or serointensity, again emphasizing that a history of other infectious
disease exposures and socioeconomic factors might inuence associations between
HTVL- 1 and neuropsychiatric outcome (Erickson et al., 2021).
Guiltinan et al. (2013) provided several mechanisms that could account for the
possible associations between HTLV- 1 and depression or anxiety. Direct physiological eects of the virus could biologically produce symptoms of depression or anxiety. Eects from the infection could produce depression or anxiety, or stress from
having a sexually transmitted disease in some cases could result in depression or
anxiety. Finally, depression or anxiety itself could increase the chance of acquiring
an infectious disease. Souza et al. (2021) suggest that the anxiety and depression that
have been associated with HTLV- 1 could be a result of what they referred to as “social vulnerability” from HTLV- 1 or a result of the neurological impairment associated with some cases of HTLV- 1, but also note the importance of considering the
role of inammation from HTLV- 1 in depression and anxiety.
Although clearly more research is needed to better understand associations between HTLV- 1 seropositivity and HAM/ TSP and depression and anxiety, the
available evidence suggests that possibly due to several as yet poorly understood
mechanisms, depression and anxiety could be a clinical feature of HTLV- 1.
Pathophysiological and neuroanatomical findings
associated with HTLV- 1
HTLV- 1 could result in neurological diseases, cognitive impairment, depression,
and anxiety via several dierent mechanisms, including direct damage to neurons
and glia, cytokine release, and induction of autoimmunity (Araujo, 2015). In a murine model, HTLV- 1 infection was associated with oxidative stress in cortical and
Infectious Disease and Neurocognition
hippocampal areas (Moghadam et al., 2018), which could be a mechanism associated with HTLV- 1’s eect on the brain. While HAM/ TSP is associated with degeneration (Grith et al., 2006) and inammatory changes in the thoracic spinal cord
(Nagai & Osame, 2003), and possibly with inammation in the brain (Dimber et al.,
2016), few studies have investigated its relationship with brain volume. In a small
study comparing 19 patients with HAM/ TSP with 14 healthy controls, there were
no dierences in overall brain volumes between the two groups. e authors, however, noted that ndings in one of the patients suggested the possibility that, in some
patients, HAM/ TSP could be associated with changes in brain volume and recommended further study (Grith et al., 2006). In a small study from Brazil, cerebral
white matter lesions were identied in a high percentage of patients with HTLV- 1—
80 percent of patients with HAM/ TSP and 85 percent of HTLV- 1 carriers (Morgan
et al., 2007). As a group, ndings from these studies suggest several mechanisms by
which HTLV- 1 might be adversely aecting brain function, although whether these
ndings account for the cognitive, depressive, and anxiety ndings associated with
HTLV- 1 is unknown. Additional research elucidating underlying mechanisms of
the association between HTLV- 1 seropositivity and cognitive and neuropsychiatric
function is needed.
Further, emphasizing the role of inammation in HAM/ TSP, cognitive function,
and depression and anxiety are associations between HTLV- 1 and inammatory disease in addition to HAM/ TSP including arthritis, polymyositis, and Sjögren’s syndrome (Nagai & Osame, 2003).
Conclusion
Increasing evidence indicates that HTLV- 1 is among the infectious diseases that
can adversely aect cognitive function and increase the risk of anxiety and depression. Although possibly due to a variety of mechanisms including inammation
(Nagai & Osame, 2003), induction of autoimmunity, direct damage to neurons and
glia (Araujo, 2015), white matter lesions (Morgan et al., 2007), or the neurological
burden associated with HTV- 1 in some cases, HTLV- 1 particularly in regions where
it is endemic appears to be associated with a high burden of neurological, neuropsychiatric, and cognitive decits. While only present in approximately 0.2– 3 percent of
people infected with HTLV- 1 (Grith et al., 2006), HAM- TSP results in signicant
changes in the thoracic spinal cord and substantial neurological impairment (Nagai
& Osame, 2003). Additional ndings further indicate that HTLV- 1 can be associated with cognitive decits not only in patients with HAM/ TSP but also in otherwise
asymptomatic carriers of HTLV- 1 (Gascón et al., 2017; Silva et al., 2003). Further,
some evidence suggests HTLV- 1 infection can be associated with depression and
anxiety in both patients with HAM/ TSP and in otherwise asymptomatic carriers
of HTLV- 1 (Gascón et al., 2011; Stumpf et al., 2008). Further, white matter lesions
occur not only in a high percentage of patients with HAM/ TSP but also in a high
Human T-Cell Lymphotropic Virus Type 1 93
percentage of HTLV- 1 carriers without HAM/ TSP (Morgan et al., 2007). As HTLV- 1
infects an estimated 5– 10 million people worldwide (Gessain & Cassar, 2012), both
HAM/ TSP and cognitive dysfunction from HTLV- 1 potentially pose considerable
clinical and public health problems.
While accumulating research ndings indicate that HTLV- 1 infection adversely aects cognitive, neurological, and neuropsychiatric health, more
research is needed to investigate how geographical region and medical, demographic, and socioeconomic variables might aect associations between HTLV- 1
seropositivity and cognitive and neuropsychiatric outcomes. Further, additional
research is required to better characterize HTLV- 1’s association with dementia,
interventions to prevent the spread of HTLV- 1, the development of safe and effective vaccines against HTLV- 1, and safe and eective treatment for HTLV- 1
infection, as well as how these interventions might prevent and treat the cognitive, neurological, and neuropsychiatric aspects of HTLV- 1. Despite its clinical
and public health burden, HTLV- 1 infection provides an opportunity to better
characterize associations between infection- induced inammatory changes and
neurocognitive and neuropsychiatric function and how medical, demographic,
and socioeconomic factor inuence associations between infectious diseases and
brain function.
References
ARAUJO, A. Q. 2015. Update on neurological manifestations of HTLV- 1 infection. Curr Infect Dis Rep,
17, 459.
BOA- SORTE, N., GALVAO- CASTRO, A. V., BORBA, D., LIMA, R. B. & GALVAO- CASTRO, B. 2015.
HAM/ TSP and major depression: e role of age. Braz J Infect Dis, 19, 314– 318.
CARON, M., BEASON, G., PADILLA, C., MAKUWA, M., NKOGHE, D., LEROY, E. & KAZANJI, M.
2018. Revisiting human T- cell lymphotropic virus types 1 and 2 infections among rural population
in Gabon, central Africa thirty years aer the rst analysis. PLoS Negl Trop Dis, 12, e0006833.
CHAMPS, A. P. S., DE AZEREDO PASSOS, V. M., CARVALHO, G., BARRETO, S. M., MEIRELLES,
C. & CARAMELLI, P. 2019. Cognitive impairment in HTLV- 1- associated myelopathy, proviral load
and inammatory markers. Int J Infect Dis, 84, 121– 126.
CHAMPS, A. P. S., PASSOS, V. M. A., BARRETO, S. M., CARAMELLI, P., DE MELO, C. M.,
CARVALHO, G., MENEZES, M. M. & RIBAS, J. G. R. 2013. Encephalomyelopathy associated with
HTLV- I: A primary disease or coexisting with multiple sclerosis? Dement Neuropsychol, 7, 439– 443.
CRAIG, A., GUEST, R., TRAN, Y. & MIDDLETON, J. 2017. Cognitive impairment and mood states
aer spinal cord injury. J Neurotrauma, 34, 1156– 1163.
DE CARVALHO, A. G., GALVÃO- PHILETO, A. V., LIMA, N. S., JESUS, R. S., GALVÃO- CASTRO,
B. & LIMA, M. G. 2009. Frequency of mental disturbances in HTLV- 1 patients in the state of Bahia,
Brazil. Braz J Infect Dis, 13, 5– 8.
DE CASTRO, A. R. R., LABANCA, L., DE RESENDE, L. M. & UTSCH- GONCALVES, D. 2020. Case
report: Cognitive impairment without clinical spinal disease may be the rst sign of HTLV- 1 neurological alteration. Am J Trop Med Hyg, 102, 366– 369.
DE PAULA, J. J., ROMANELLI, L. C., DE FARIA, R. C. V., PROIETTI, A. B., MALLOY- DINIZ, L. F.,
ROMANO- SILVA, M. A., DE MIRANDA, D. M. & NICOLATO, R. 2021. Cognitive impairment in
the HTLV- 1 infection: A comparative study associated with functional performance. J Neurovirol,
27, 849– 856.
Infectious Disease and Neurocognition
DIMBER, R., GUO, Q., BISHOP, C., ADONIS, A., BUCKLEY, A., KOCSIS, A., OWEN, D., KALK,
N., NEWBOULD, R., GUNN, R. N., RABINER, E. A. & TAYLOR, G. P. 2016. Evidence of brain inammation in patients with human T- lymphotropic virus type 1- associated myelopathy (HAM): A
pilot, multimodal imaging study using 11C- PBR28 PET, MR T1- weighted, and diusion- weighted
imaging. J Nucl Med, 57, 1905– 1912.
ERICKSON, L. D., HEDGES, D. W., BROWN, B. L., EMBLEY, B. & GALE, S. D. 2021. Association be-
tween cognitive function and depression with human T- cell lymphotropic virus 1 seropositivity and
serointensity in UK adults. Pathogens, 10, 1409.
GASCÓN, M. R. P., CAPITAO, C. G., CASSEB, J., NOGUEIRA- MARTINS, M. C. F., SMID, J. & DE
OLIVEIRA, A. C. P. 2011. Prevalence of anxiety, depression and quality of life in HTLV- 1 infected
patients. Braz J Infect Dis, 15, 578– 582.
GASCÓN, M. R. P., CASSEB, J., SMID, J., VIDAL, J. E., FONSECA, L. A. M., PAIVA, A., HAZIOT, M.
J. & PENALVA DE OLIVEIRA, A. C. 2017. Cognitive impairment is frequent among symptomatic
carriers of human T- cell lymphotropic virus type 1 (HTLV- 1), regardless of their clinical status. J
Neurol Sci, 377, 185– 189.
GESSAIN, A. & CASSAR, O. 2012. Epidemiological aspects and world distribution of HTLV- 1 infec-
tion. Front Microbiol, 3, 388.
GONCALVES, L. R., BARBOSA, L. N. F., MAGALHAES, P. M. R. & ROCHA, P. A. S. 2017.
Characterization of cognitive performance and evaluation of quality of life among patients with
HTLV- 1. Clin Neurol Neurosurg, 160, 142– 146.
GRIFFITH, C., BAGNATO, F., GUPTA, S., CALABRESE, A., OH, U., CHIU, A., OHAYON, J. M.,
MCAULIFFE, M. J., TASCIYAN, T. A. & JACOBSON, S. 2006. Brain volume measurements in patients with human T- cell lymphotropic virus- 1- associated tropical spastic paraparesis. J Neurovirol,
12, 349– 355.
GUILTINAN, A. M., KAIDAROVA, Z., BEHAN, D., MAROSI, C., HUTCHING, S., KAISER, M.,
MOORE, E., DEVITA, D., MURPHY, E. L. & HTLV OUTCOMES STUDY (HOST). 2013. Major
depression and generalized anxiety disorder among human T- lymphotropic virus types I- and IIinfected former blood donors. Transfusion, 53, 60– 68.
HAZIOT, M. E., GASCÓN, M. R., ASSONE, T., FONSECA, L. A. M., LUIZ, O. D. C., SMID, J., PAIVA,
A. M., MARCUSSO, R., DE OLIVEIRA, A. C. P. & CASSEB, J. 2019. Detection of clinical and neurological signs in apparently asymptomatic HTLV- 1 infected carriers: Association with high proviral
load. PLoS Negl Trop Dis, 13, e0006967.
HOLUKA, C., MERZ, M. P., FERNANDES, S. B., CHARALAMBOUS, E. G., SEAL, S. V., GROVA, N. &
TURNER, J. D. 2020. e COVID- 19 pandemic: Does our early life environment, life trajectory and
socioeconomic status determine disease susceptibility and severity? Int J Mol Sci, 21, 5094.
KENDALL, E. A., GONZÁLEZ, E., ESPINOZA, I., TIPISMANA, M., VERDONCK, K., CLARK, D.,
VERMUND, S. H. & GOTUZZO, E. 2009. Early neurologic abnormalities associated with human
T- cell lymphotropic virus type 1 infection in a cohort of Peruvian children. J P edia tr, 155, 700– 706.
KIRA, J., HAMADA, T., KAWANO, Y., OKAYAMA, M. & YAMASAKI, K. 1997. An association of
human T- cell lymphotropic virus type I infection with vascular dementia. Acta Neurol Scand, 96,
305– 309.
MOGHADAM, M. H., REZAEE, S. A. R., HOSSEINI, M., NIAZMAND, S., SALMANI, H.,
RAFATPANAH, H., ASARZADEGAN DEZFULI, M., AMEL ZABIHI, N., ABARESHI, A. &
MAHMOUDABADY, M. 2018. HTLV- 1 infection- induced motor dysfunction, memory impairment, depression, and brain tissues oxidative damage in female BALB/ c mice. Life Sci, 212, 9– 19.
MORGAN, D. J., CASKEY, M. F., ABBEHUSEN, C., OLIVEIRA- FILHO, J., ARAUJO, C., PORTO,
A. F., SANTOS, S. B., ORGE, G. O., JOIA, M. J., MUNIZ, A. L., SIQUEIRA, I., GLESBY, M. J. &
CARVALHO, E. 2007. Brain magnetic resonance imaging white matter lesions are frequent in HTLVI carriers and do not discriminate from HAM/ TSP. AIDS Res Hum Retroviruses, 23, 1499– 1504.
NAGAI, M. & OSAME, M. 2003. Human T- cell lymphotropic virus type I and neurological diseases. J
Neurovirol, 9, 228– 235.
NOSE, H., SAITO, M., USUKU, K., SABOURI, A. H., MATSUZAKI, T., KUBOTA, R., EIRAKU, N.,
FURUKAWA, Y., IZUMO, S., ARIMURA, K. & OSAME, M. 2006. Clinical symptoms and the odds
of human T- cell lymphotropic virus type 1- associated myelopathy/ tropical spastic paraparesis
Human T-Cell Lymphotropic Virus Type 1 95
(HAM/ TSP) in healthy virus carriers: Application of best- t logistic regression equation based on
host genotype, age, and provirus load. J Neurovirol, 12, 171– 177.
ROCHA- FILHO, P. A. S. & GONCALVES, L. R. 2018. Depression and anxiety disorders among pa-
tients with human T- cell lymphotropic virus type- 1: A cross- sectional study with a comparison
group. Rev Soc Bras Med Trop, 51, 357– 360.
ROSADAS, C., ASSONE, T., YAMASHITA, M., ADONIS, A., PUCCIONI- SOHLER, M., SANTOS,
M., PAIVA, A., CASSEB, J., OLIVEIRA, A. C. P. & TAYLOR, G. P. 2020. Health state utility values in
people living with HTLV- 1 and in patients with HAM/ TSP: e impact of a neglected disease on the
quality of life. PLoS Negl Trop Dis, 14, e0008761.
SAITO, M. 2019. Association between HTLV- 1 genotypes and risk of HAM/ TSP. Front Microbiol,
10, 1101.
SILVA, M. T. T., MATTOS, P., ALFANO, A. & ARAUJO, A. Q. C. 2003. Neuropsychological assessment
in HTLV- 1 infection: A comparative study among TSP/ HAM, asymptomatic carriers, and healthy
controls. J Neurol Neurosurg Psychiatry, 74, 1085– 1089.
SOUZA, L. S., LINS- SILVA, D. H., DOREA- BANDEIRA, I., BAROUH, J. L., TOLENTINO, A.,
BANDEIRA, I. D. & QUARANTINI, L. C. 2021. Prevalence and factors associated with depression and anxiety in people living with HTLV- 1: A systematic review with meta- analysis and metaregression. Gen Hosp Psychiatry, 73, 54– 63.
STUMPF, B. P., CARNEIRO- PROIETTI, A. B., PROIETTI, F. A., ROCHA, F. L. & INTERDISCIPLINARY,
H. R. G. 2008. Higher rate of major depression among blood donor candidates infected with human T- cell
lymphotropic virus type 1. Int J Psychiatry Med, 38, 345– 355.
VASCONCELOS, B. H. B., CALLEGARI, B., COSTA, K. H. A., BARROSO, T. G. C. P., SOUSA, R.
C. M., SAUNIER, G., XAVIER, M. B. & SOUZA, G. S. 2019. Balance impairments in patients with
human T- cell lymphotropic virus type 1 infection. Sci Rep, 9, 11456.
PART II
BACTERIAL DISEASES
IN NEUROCOGNITIVE AND
NEUROPSYCHIATRIC MEDICINE