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DEPRESSIVE SYMPTOMS AND CERVICAL NEOPLASIA IN HIV+ WOMEN WITH
HUMAN PAPILLOMAVIRUS INFECTION
STACY MARIE DODD
A THESIS PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF SCIENCE
UNIVERSITY OF FLORIDA
O 2007 Stacy Marie Dodd
To Jeriann Dodd
First, I thank Dr. Deidre Pereira for her mentorship, guidance, and support throughout the
many phases of this proj ect. Her depth of knowledge, insightful advice, and passion for research
has been instrumental in the completion of this work. I thank Dr. Michael Antoni, the principle
investigator on this study, for allowing me to participate in this research. Additionally, I extend
my appreciation to Ms. Sally Jensen, who has served as an excellent role model and provided
guidance throughout this process. I would like to thank Ms. Ilona Buscher, Dr. Michele Peake,
Ms. Trudi Simon, Dr. Mary Ann Fletcher, and Dr. Kevin Maher at the University of Miami for
their involvement in this study. I also acknowledge the members of my committee, Dr. Samuel
Sears, Dr. Dawn Bowers, and Dr. Stephen Boggs.
I would like to thank my family, and specifically my parents, for their endless support.
Without my mother and father none of this would have been possible. I thank my mother for
being my inspiration for pursuing research in this field. I would also like to thank my friends
and classmates for their guidance and support as well as camaraderie throughout this process.
I extend my great appreciation for all of the women who participated in this research. I
wish them the best.
TABLE OF CONTENTS
ACKNOWLEDGMENTS .............. ...............4.....
LIST OF TABLES ................ ...............7............ ....
AB S TRAC T ......_ ................. ............_........8
1 INTRODUCTION ................. ...............10.......... ......
Epidemiology of HIV ............. ..... __ ...............10..
Pathophysiology ofHIV/AIDS............... ...............1
HIV/AIDS Classification............... .............1
HIV and Human Papillomavirus .............. ...............12....
Psychoneuroimmunology and CIN................ ...............13..
Depression and HIV .............. ...............14....
Current Study ................. ...............15.......... ......
2 METHODS ................. ...............17.......... .....
Design ................. ...............17.................
Participants .............. ...............17....
Proc edure s ................ ...............18........... ....
Screening Visit .............. ...............18....
Psychosocial Interview............... ...............1
Statistical Procedures............... ...............1
3 RE SULT S .............. ...............21....
Demographics ................. ...............21.................
Health Behaviors .............. ...............21....
Health Status ................. ...............22.................
Depressive Symptoms ............... ......... .............. .......2
Relations between Depressive Symptoms and HIV-Related Immunity ............... .................22
Relations between Biobehavioral Variables and Cervical Neoplasia............... ................2
Relations between Depressive Symptomatology and Cervical Neoplasia .............................23
4 DI SCUS SSION .........__. ....._..... ...............29....
Study Limitations. ........._.._.. ...._... ...............3 1....
Future Directions .............. ...............32....
LIST OF REFERENCES ................. ...............35................
BIOGRAPHICAL SKETCH .............. ...............41....
LIST OF TABLES
1-1 CDC classification ofHIV/AIDS. ............. ...............16.....
3-1 Comparison of continuous demographic and health variables in participants who
provided full and partial data. .............. ...............25....
3-2 Comparison of categorical demographic and health variables in participants who
provided full and partial data. .............. ...............25....
3-3 Predicting presence of cervical neoplasia from depressive symptoms. .............................26
3-4 Predicting presence of cervical neoplasia from cognitive/affective depressive
sym ptom s. ............. ...............27.....
3-5 Predicting presence of cervical neoplasia from somatic depressive symptoms. ...............28
Abstract of Thesis Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Master of Science
DEPRESSIVE SYMPTOMS AND CERVICAL NEOPLASIA IN HIV+ WOMEN WITH
HUMAN PAPILLOMAVIRUS INFECTION
Stacy Marie Dodd
Chair: Deidre Pereira
Prior work has related elevated life stress to greater risk of cervical neoplasia in women co-
infected with human immunodeficiency virus (HIV) and human papillomavirus (HPV). This
study investigated associations between depressive symptoms (independent of life stress and
other possible confounders) and cervical neoplasia in women with HIV and HPV infection.
Participants for this study were 54 HIV+HPV+ women; most were African American.
Participants underwent a colposcopy, HPV screening, Papanicolaou smear, and cervical biopsy
to determine study eligibility. Eligible participants then completed the Beck Depression
Inventory (BDI). Scores on the BDI were used as a whole and were also divided into
cognitive/affective symptoms and somatic symptoms. Hierarchical logistic regression analysis
revealed that women who reported more depressive symptoms had marginally greater odds of
presenting with cervical neoplasia, OR = 1.32, p = .062. While cognitive and affective
depressive symptoms were not significantly associated with greater odds of presenting with
cervical neoplasia, women who reported more somatic depressive symptoms had greater odds of
presenting with cervical neoplasia, OR = 2.29 p = .022, even after controlling for biobehavioral
risk factors for cervical neoplasia (HIV viral load and high-risk HPV) and recent negative life
events. Thus, women who reported more somatic depressive symptoms had greater odds of
presenting with cervical neoplasia. These findings may suggest that screening HIV+ women for
somatic depression may help identify those at risk for cervical neoplasia. In addition, these
findings suggest that future research on depression in medical populations should not ignore
somatic depressive symptoms, as they may have important implications for health outcomes.
Epidemiology of HIV
Human immunodeficiency virus (HIV) is the virus that causes acquired
immunodeficiency syndrome (AIDS). HIV and AIDS are serious global health threats. In 2003,
an estimated 4.8 million people worldwide became newly infected with HIV. Approximately
37.8 million people are currently living with HIV. Over 20 million have died from the disease
since the epidemic began in 1981; 2.9 million died in 2003 alone (Joint United Nations
Programme on HIV/AIDS [UNAIDS], 2004). In the United States, 43,171 new AIDS cases
were reported to the Center for Disease Control and Prevention (CDC) in 2003. Of these, 21,304
(49.3%) cases were diagnosed in African Americans compared to 12,222 (28.3%) cases
diagnosed in Caucasians. AIDS-related mortality is also higher among African Americans than
Caucasians. Death rates associated with AIDS are nearly 8 times higher in African American
men than Caucasian men. For women the disparity was even larger: death rates for African
American women due to AIDS are nearly 13 times higher than those for Caucasian women
(National Center for Health Statistics, 2005). In 2002, HIV/AIDS was the leading cause of death
in African American women between the ages of 25 and 34 (Anderson & Smith, 2005). These
discrepancies are even more pronounced since African Americans constitute only 12.3% of the
U.S. population (U.S. Census Bureau data for 2000, 2006). Although HIV and AIDS are serious
health threats for all Americans, the virus and disease have a disproportionately large impact on
the African American community.
Pathophysiology of HIV/AIDS
Infection with HIV occurs through mucosal contact with bodily fluids infected with the
virus. This occurs through sexual intercourse or the sharing of contaminated needles. In the past,
HIV infection occurred following medical transfusion of infected blood products; this has
become rare subsequent to blood screening procedures to identify infected blood. Approximately
2-6 weeks following initial infection, most (but not all) individuals experience an influenza-like
illness corresponding with the initiation of HIV-specific cellular immune responses (Nadler,
2006). During this time, cytotoxic T-cells (CD8 T-cells) are activated and work to kill HIV
infected cells and HIV antibody production occurs (Janeway, Travers, Walport & Shlomchik,
After the primary infection stage, HIV enters the second stage of infection, often referred
to as the asymptomatic stage. Though individuals in this stage generally do not express any
clinical symptoms, the virus continues to replicate and CD4 T-cell counts continue to decline
(Nadler, 2006). One of the primary factors influencing the amount of time an individual remains
in the asymptomatic stage is the initial effectiveness of the immune response to contain the
infection. The HIV viral load that is established subsequent to initial infection remains fairly
stable over several years, and those with the highest viral loads generally have faster progressing
HIV infection (Nadler, 2006). For most individuals, this second stage of HIV infection
eventually progresses to clinical AIDS, which is characterized by low CD4 cell counts and/or the
development of an AIDS-defining illness, as described below.
In 1993, the CDC revised the classification system for HIV/AIDS. According to the
revisions, HIV/AIDS is classified using three ranges of CD4 cell counts and three clinical
The three ranges of CD4 cell counts used to classify HIV infection are 500 cells/CIL or
greater (Category 1), 200-499 cells/CIL (Category 2), and less than 200 cells/CIL (Category 3).
Individuals in Category 3 are classified as having developed AIDS, regardless of whether they
have developed an AIDS defining condition. Category determinations are made based upon the
lowest accurate CD4 cell count for that individual, which is not necessarily the most recent cell
count obtained (CDC, 1992).
The three clinical categories of HIV/AIDS are Category A, B, and C. An individual is
categorized as being in Category A, or asymptomatic HIV, if they have never experienced a
symptomatic AIDS condition or an AIDS-defining illness (described below). Category B, or
symptomatic HIV, is assigned to individuals who have experienced a symptomatic condition
occurring in an HIV infected individual that is either attributed to the HIV infection or indicates
a deficit in cell-mediated immunity, or conditions that have a clinical course that is complicated
by the HIV infection. These do not include conditions designated as AIDS-defining illnesses.
Category C, or clinical AIDS, is reached when an individual experiences an AIDS-defining
illness as defined by the CDC. Classifieation of the clinical categories are based upon the history
of HIV progression, thus once an individual meets criteria for a category they cannot move back
into a previous category, even if the symptoms or illness placing them in the category is resolved
Based upon the three CD4 cell count categories and the three clinical categories, there are
nine mutually exclusive categories for the staging of HIV/AIDS, ranging from Al-C3 (Table 1-
2). Categories A3, B3, C3, C1, and C2 confer a diagnosis of AIDS.
HIV and Human Papillomavirus
HIV infection may have a different course in women compared to men. Specifically,
several opportunistic illnesses are more common, harder to treat, or occur exclusively in women
with HIV as compared to their male counterparts. Examples include disorders of the upper
genital tract, such as pelvic inflammatory disease, as well as disorders of the lower genital tract,
such as cervical intraepithelial neoplasia (CINT) (CDC, 1992). CIN is the pre-malignant phase of
cervical cancer that is initiated and promoted to cervical cancer by oncogenic Human
Papillomavirus (HPV) infection, including HPV 16 and 18 infections. HPV is one of the most
common sexually transmitted infections in the United States. Among immunocompetent women
with HPV infection, adequate cellular immune responses, most notably T helper type 1 (Thl)
cell immune responses (Scott, Stites, & Moscicki, 1999), will survey the virus before it promotes
the pre-malignant or malignant transformation of cells (Munoz et al., 2003). However, HPV
infected women with suppressed cellular immune responses, such as women with
immunodeficiency due to HIV infection, are not able to mount an adequate immune defense
against HPV, resulting in persistent and severe HPV infection and risk for malignant
transformation of cells. Additional risk factors for CIN and cervical cancer among women with
HIV include degree of immunosuppression (low T helper/inducer lymphocyte [CD4+CD3+] cell
counts) (Phelps et al., 2001; Davis et al., 2001), tobacco smoking (Hocke et al., 1998), and
uncontrolled HIV viral load (Davis et al., 2001).
Psychoneuroimmunology and CIN
Pyschoneuroimmunology (PNI) is the investigation of the relations among psychosocial
variables, neuroendocrine and immunologic functioning, and health outcomes. Research
investigating psychosocial variables and the presence and/or persistence of CIN has yielded
inconsistent results. Previous research has shown that poorer psychological well-being (greater
pessimistic attitude, greater negative life event stress) is associated with lower cell-mediated and
natural immunity (Byrnes et al., 1998), greater number of genital herpes recurrences (Pereira et
al., 2003b), and greater odds of progression and/or persistence of cervical neoplasia (Pereira et
al., 2003a) in women with HIV and HPV infections. In contrast, other researchers have reported
no associations between CIN progression or regression with negative life events, lack of social
support, or coping style (Tiersma et al., 2005; Tiersma et al., 2004). However, no research to
date has explored whether other common and treatable psychological conditions, such as
depression, are associated with cervical neoplasia in women with HIV and HPV infections.
Depression and HIV
The relationship between depression and health status in HIV+ women is particularly
important to examine for several reasons. Depressive symptoms and disorders are common
among individuals with HIV infection. Studies have shown that nearly half of individuals with
HIV infection meet diagnostic criteria for depression (Chandra et al., 1998). HIV+ women may
be at particularly high risk of experiencing depressive symptoms. Studies have shown that
women in the general population experience maj or depression twice as often as men (Weissman
& Off son, 1995), and women infected with HIV experience maj or depression significantly more
often than healthy women (Morrison et al., 2002). In addition, HIV+ women experience
depression at rates twice that of HIV+ men (Evans et al., 2002). Notably, depressive symptoms
in HIV+ individuals are associated with more rapid decline of CD4+CD3+ cell counts (Rabkin et
al., 1991; Lyketsos et al., 1993; Sahs et al., 1994; Vedhara, Schifitoo, & McDermott, 1999;
Burack et al., 1993; Ickovic et al., 2001), decreased natural killer (NK) cell activity, increased
HIV viral load, and greater risk of HIV related mortality (Burack et al., 1993; Ickovics et al.,
2001; Mayne et al., 1996; Leserman et al., 1999). Depressive symptoms are also associated with
faster development of any AIDS defining condition (Leserman et al., 2002).
In spite of this research, no research to our knowledge has investigated the possible
relationship between depressive symptoms and cervical neoplasia, a female-specific HIV
associated opportunistic illness. This relationship is of particular interest, because susceptibility
to depression is elevated among women experiencing high life stress (Kendler, Karkowski, &
Prescott, 1999) and individuals who are dispositionally pessimistic (Beck, 1967; Pyszcynski,
Holt, & Greenberg, 1987), two psychosocial factors previously associated with lowered
immunity and progression and/or persistence of cervical neoplasia in HIV+ HPV+ women
(Byrnes et al., 1998; Pereira et al., 2003).
The purpose of the current study was to determine whether recent depressive symptoms
were associated with the presence of cervical neoplasia in a sample of primarily Black/African
American women with HIV and HPV infections recruited for a trial examining the effect of a
cognitive behavioral stress management (CBSM) intervention on health (e.g., cervical neoplasia)
and quality of life outcomes. It was specifically hypothesized that women with greater recent
depressive symptomatology would have greater odds of cervical neoplasia at study entry. Given
that HIV-related symptoms and medication side effects may be confounded with somatic
symptoms of depression (Blaney et al., 2004; Jones, Beach, & Forehand, 2001), we also
examined whether greater cognitive/affective symptoms of depression, specifically, were
associated with greater odds of cervical neoplasia.
Table 1-1 CDC classification ofHIV/AIDS.
A (Asymptomatic HIV) HIV)
1 500 or greater cells/ CIL Al Bl
2 200-499 cells/CIL A2 B2
3 less than 200 cells/CIL A3 B3
Note: Categories A3, B3, C3, Cl and C2 receive a diagnosis of AIDS.
The current study utilized a cross-sectional design. Fifty-four women co-infected with HIV
and HPV underwent a colposcopy, HPV testing and subtyping, a peripheral venous blood draw,
urine collection, and a 60-90 minute psychosocial interview assessing mood and health
behaviors. Statistical analyses examined the relationships between depressive symptomatology
and the presence or absence of cervical neoplasia at study entry, while controlling for known
biobehavioral risk factors for cervical neoplasia.
Participants for this study were recruited as part of a longitudinal National Cancer
Institute (NCI) funded study investigating the effects of a cognitive-behavioral stress
management (CBSM) intervention on the health and quality of life of women with HIV at risk
for cervical cancer (PI: Michael H. Antoni, Ph.D., 5 P50 CA 084944-05). Inclusion criteria
were: (a) HIV+ women ages 18 to 60 years old, (b) history of at least 2 Papanicolaou smears
indicating low grade squamous intraepithelial lesions (LSIL) or 2 cervical biopsies indicating
CINT I in the 2 years prior to study entry, and (c) fluency in spoken English. Exclusion criteria
were: (a) 2 or more negative Papanicolaou smears in the 2 years prior to study entry, (b) any
history of high grade SIL (HSIL) or any history of CIN II, CIN III, or invasive cervical cancer,
(c) any diagnostic or treatment procedures for CIN in the 6 months prior to study entry, (d) life
expectancy < 12 months as determined by the study's research nurse, and (e) current maj or,
severe psychiatric illnesses that would interfere with the ability to provide valid psychosocial
assessment data (e.g., suicidality, psychoticism, HIV dementia).
Participants for this study were recruited through Special Immunology Clinics at the
University of Miami/Jackson Memorial Hospitals. Patients at the Special Immunology Clinics
were initially screened based on medical record data to determine whether they met basic
eligibility requirements. If a patient passed the preliminary eligibility screening, a researcher
approached her during her visit to the clinic and explained the study. Patients that were
interested in participating in the study were scheduled to come in for a formal screening
At the formal screening appointment, the study was explained in more detail and
informed consent was completed. In addition, the participant provided information on her
gynecologic history, underwent a psychological screening, was provided an educational module
regarding colposcopies, and a colposcopy was performed. The colposcopy was comprised of a
Papanicolaou smear, colposcopic-guided cervical biopsy, and cervical swab for the detection and
subtyping of HPV infection. Based on the results of the colposcopy, participants were classified
as being positive or negative for cervical neoplasia at study entry. Hybrid Capture (HC) II assay
(Digene Corporation, Gaithersburg, MD) was used to classify HPV subtypes as intermediate to
high risk HPV (oncogenic subtypes) or low risk HPV subtypes. Immediately following the
colposcopy, participants were administered the Psychosocial Effects of Abnormal Pap Smears
Questionnaire (PEAPS-Q Bennetts et al., 1995) to measure distress related to the colposcopy.
Participants also underwent a peripheral venous blood draw in order to measure CD4+CD3+ cell
counts and plasma HIV viral load. At the end of this visit, participants were given urine
collection materials and instructions on collecting urine before their next visit. They were then
contacted approximately one week later with the results of the screening and to inform them of
whether or not they were ultimately eligible to participate in the study.
If the participant was eligible for study participation after the formal screening, she was
scheduled for another visit. At this visit, participants completed a psychosocial assessment
interview. This interview included the Beck Depression Inventory (BDI Beck, Ward,
Mendelson, Mock & Erbaugh, 1961) and a general demographic questionnaire, among other
psychosocial measures. The BDI is a 21-item self-report questionnaire that measures symptoms
of depression. The BDI has been used extensively in previous research investigating depressive
symptoms in HIV+ populations (Castellon, Hinkin, Wood & Yarema, 1998; Ferrando, Rabkin,
de Moore & Rabkin, 1999; Judd et al., 2005; Laperriere et al., 2005; Weiser et al., 2006).
Questions on the BDI assess both cognitive and affective (e.g., sadness, hopelessness) as well as
somatic (e.g. fatigue, weight change) depressive symptoms. Thus it is possible to create scale
scores from the BDI, which measure an individual's levels of cognitive/affective and somatic
depressive symptoms independently.
Results presented in this paper are based upon cross-sectional psychosocial (i.e., BDI
scores) and biological (i.e., cervical neoplasia) data. We started by examining relations between
potential demographic and biobehavioral control variables and cervical neoplasia in this sample.
We then examined the relationship between recent depressive symptoms and the presence of
cervical neoplasia in women with HIV and HPV infection using hierarchical logistic regression.
Regression equations contained two blocks of predictor variables: the first block consisted of
traditional, well-established risk factors for cervical neoplasia in HIV+ women (CD4+CD3+ cell
count, HIV viral load, HR-HPV infection, and tobacco smoking) (Davis et al., 2001; Hocke et
al., 1998; Phelps et al., 2001), and the second block consisted of our psychosocial predictor of
interest scores on the BDI. Two hierarchical logistic regression equations were analyzed. The
first equation contained scores from all 21 items of the BDI. The second equation contained
scores from only the cognitive/affective items of the BDI (i.e., BDI items 1 15). The criterion
in both equations was presence ("1") or absence ("O") of cervical neoplasia by histology
(cervical biopsy) at study entry. If a cervical biopsy was clinically contraindicated for a
particular participant, the presence or absence of squamous intraepithelial lesions (SIL) by
cervical cytology (Papanicolaou smear) at study entry was used.
Sixty-six women met study criteria and were enrolled in this study. The results reported
here are based on 54 participants who provided full psychosocial, colposcopic, and immune data.
Results of t-tests and chi-square analyses revealed that participants who provided complete data
did not differ significantly (p > .05) from those who had incomplete data in age, yearly income,
years of education, ethnicity, marital status, presence of neoplasia, presence of high-risk HPV,
HIV stage, or CD4+CD3+ cells/mm3. (Tables 3-1 & 3-2).
The 54 participants who provided full data ranged in age from 18-45 years (M = 30 years,
SD = 8.5 years). The majority of the women were non-Hispanic Black/African American
(85.2%), with the remainder of the sample being comprised of Hispanic Caucasian (9.3%), non-
Hispanic Caucasian (3.7%), and other (1.9%). The women had an average yearly income of
$11,601 (S = $8,089), and averaged 11.6 years of education (SD = 1.23 years). The majority
of women in the study (55.6%) were single/never married. Of the remaining 44.4%, 20.4% were
married or in an equivalent relationship and 24% were separated, divorced, or widowed.
Seventy-two percent of the women who participated in this study were taking highly
active anti-retroviral therapy (HAART) at the time of study entry. Self-reported adherence to
HAART was significantly negatively correlated with HIV viral load, r = -.413, p = .011. Nearly
60% of the participants reported never having smoked. Of the remaining women who did report
a history of smoking (N = 22), pack-years of smoking ranged from 6 5,110 (M = 1,904, SD =
Colposcopic-guided cervical biopsy revealed that 44 women (81.5%) presented with
cervical neoplasia at study entry, while 10 women (18.5%) did not show evidence of cervical
neoplasia. HPV screening and typing revealed that 42 women (77.7%) tested positive for
intermediate or HR-HPV types.
Twenty-three women (42.6%) had Category A (asymptomatic) disease at study entry.
Thirteen women (24. 1%) had Category B (symptomatic) disease, and 17 women (31.5%) had
Category C (clinical AIDS) disease. The mean CD4+CD3+ cells/mm3 was 455.43 (SD =
285.47). Eight women (14.8%) had CD4+CD3+ cell counts below 200 cells/mm3, 27 women
(50%) had cell counts between 200 and 500 cells/mm3, and 19 women (35.2%) had cell counts
above 500 cells/mm3
Possible scores on the BDI range from 0-63, with higher scores indicating more depressive
symptoms reported. The women in this study scored between 0-44 on the full BDI, with a mean
of 8.6 (jS = 9.81). Previous research with HIV populations has utilized a BDI cutoff score of 10
to indicate depression (Laperriere et al., 2005), thus the average score for women in this study
was below depression cutoffs on the BDI. Twenty-one women (39%) in the study obtained BDI
scores of 10 or greater.
Relations between Depressive Symptoms and HIV-Related Immunity
The results of correlational analyses demonstrated that neither total BDI scores nor
cognitive/affective BDI scores were correlated with CD4+CD3+ cell counts; however, women
with greater somatic BDI scores had significantly lower CD4+CD3+cell counts, r = -.286, p =
.036. BDI scores (total, cognitive/affective, and somatic) and HIV viral load were not correlated
(P's > .05).
Relations between Biobehavioral Variables and Cervical Neoplasia
Correlational and chi-squared analyses were conducted to determine whether variables that
have been shown to be risk factors of cervical neoplasia in HIV+ women (HIV viral load,
presence of HR-HPV subtypes, CD4+CD3+ cell counts, and tobacco smoking) were related to
cervical neoplasia in this sample. HIV viral load (r = .30, p = .027) and presence of HR-HPV
subtypes (E  = 5.48, p = .019) were significantly related to the presence of neoplasia. Despite
the fact that CD4+CD3+ cell counts and tobacco smoking were not significantly related to
neoplasia, all four potential risk factors were entered as control variables into Block 1 of the
regression equations as a conservative measure based on their strong associations with incidence
of neoplasia in previous research.
Relations between Depressive Symptomatology and Cervical Neoplasia
Using scores from the entire BDI as the predictor of interest, a marginally significant
relationship emerged between greater depressive symptomatology and greater odds of cervical
neo lasia, OR = 1.19, 95% CI = .0.98 1.45, = .084. The overall model was si nificant, 2 5
= 16.72, 12 = 0.005 (Table 3-3). Subsequently, the relationship between only the
cognitive/affective items of the BDI, specifically, and cervical neoplasia was examined.
Contrary to our hypothesis, there was no significant relationship between cognitive/affective
s mtoms of d pression and the odds of cervical neo lasia, OR = 1.18, 95% CI = 0.95 1.48,
= 0.181 (Table 3-4).
Given that there was (a) a marginally significant relationship between scores on the entire
BDI and cervical neoplasia and (b) no significant relationship between the cognitive/affective
scores and neoplasia, we explored the possibility that scores on the somatic items of the BDI
(BDI items 16-21) were related to greater odds of cervical neoplasia. Hierarchical logistic
regression analysis revealed that women who reported higher levels of recent somatic depressive
symptomatology had over two-fold greater odds of cervical neoplasia, OR = 2.21, 95% CI = 1.03
- 4.73, p = 0.042. The overall model was significant, 2C (5) = 19.77 p = 0.001 (Table 3-5). In
order to ensure that the relationship between recent somatic depressive symptoms and cervical
neoplasia was independent of life stress, a factor previously demonstrated to be associated with
the progression and/or persistence of cervical neoplasia in HIV+ women over time (Pereira et al.,
2003), we also controlled for the impact of recent negative life event stress using an abbreviated
10-item version of the Life Experiences Survey (LES) (Sarason, Johnson, & Seigel, 1978)
described in detail elsewhere (Pereira et al., 2003). A significant relationship remained between
greater somatic depressive symptoms and greater odds of cervical neoplasia after controlling for
risk factors for neo lasia and life stress, OR = 2.19, 95% CI = 1.01 4.74, = 0.046 (not
Finally, to investigate whether an individual somatic depressive symptom was driving the
association between somatic depressive symptomatology and cervical neoplasia, correlational
analyses were conducted on each of the somatic BDI items and neoplasia. Results of these
analyses showed that only the BDI question regarding difficulty sleeping was significantly
correlated with cervical neoplasia (r = .313, p = .021). However, when the BDI question
regarding sleep was removed from the hierarchical logistic regression, the remaining somatic
depressive symptoms continued to be significantly associated with greater odds of presenting
with cervical neo lasia (OR = 2.27, = .049, 95% CI = 1.01-5.12 Thus, it a pears that the
constellation of somatic depressive symptoms and not necessarily difficulty sleeping is
associated with greater odds of presenting with cervical neoplasia.
Table 3-1 Comparison of continuous demographic and health variables in participants who provided full and partial data.
Yearly income ($)
Years of education
HIV viral load
1.75 (2.18) -1.138
Table 3-2 Comparison of categorical demographic and health variables in participants who provided full and partial data.
Variable r/ df p value
Race 4.298 7 0.745
Marital status 2.75 4 0.601
Presence of dysplasia 0.578 1 0.447
HIV clinical axis .535 2 0.765
HPV status 1.667 1 0.197
Table 3-3 Predicting presence of cervical neoplasia from depressive symptoms.
(Step number) Wald Odds p 95% confidence
predictor B statistic ratio Value interval
HIV viral load
transformed]) .476 3.151 1.609 0.076 0.
High-risk HPV 1.634 3.007 5.126 .083.
(cells/mm3) 0.000 0.057 1.000 0.812 0.
Smoking .001 2.103 1.001 0.147 1.
(2) Psychological variable
Full BDI score 0.175 2.977 1.191 .084 0.
N = 54. Significance of the model, X2 (5) = 16.724, p = .005. Nagelkerke R2 = .432
Table 3-4 Predicting presence of cervical neoplasia from cognitive/affective depressive symptoms.
(Step number) Wa
HIV viral load
High-risk HPV 1.585
(2) Psychological variable
BDI score .169
N = 54. Significance of model, X2 (5)
p value interval
3.462 1.627 0.063
3.036 4.88 0.081
0.040 1.000 0.841
2.486 0.1.001 .115
2.266 1.184 0.132
14.953, p =.011. Nagelkerke' s R2
Table 3-5 Predicting presence of cervical neoplasia from somatic depressive symptoms.
(Step number) W
HIV viral load
High-risk HPV 1.307
(2) Psychological variable
Somatic BDI score 0.791
N = 54. Significance of model, X2 (5)
p value interval
.001. Nagelkerke's R2 = .497
Previous research has shown that depression and depressive symptoms are associated
with negative health outcomes for individuals with HIV infection (Burack et al., 1993; Ickovics
et al., 2001; Mayne et al., 1996; Leserman et al., 1999; Leserman et al., 2002). However, very
little research has investigated the possible relationship between depressive symptoms and HIV-
specific pathophysiologic disease processes in women. This is a significant gap in the current
literature, because the relationship between depression and specific HIV disease outcomes may
help to explain the associations that have already been demonstrated between depression and
more global yet highly significant outcomes, such as HIV progression and mortality. By
identifying the specific disease processes that may underlie the previously demonstrated link
between depression and HIV progression and mortality, specific screening and interventions can
be tailored to provide the most effective and comprehensive treatments for HIV+ women.
The current study is the first, to our knowledge, to examine the relationship between
depressive symptoms and HPV-initiated cervical neoplasia, the pre-malignant stage of cervical
cancer. Cervical cancer is the most common AIDS defining malignancy in women with HIV
infection (Maiman et al., 1997). The progression of cervical neoplasia in HIV+ women has
significant clinical implications, as CINT II advances HIV+ women to symptomatic disease status
and CINT III advances HIV+ women to a clinical AIDS diagnosis. Fortunately, cervical neoplasia
is easily detectable via cervical cytology and histology, thus allowing for the initiation of
treatment prior to the development of invasive cervical cancer. In addition, cervical neoplasia is
initiated by HPV infection, a common, sexually-transmitted virus that is controlled by the
immune system and, by implication, potentially influenced by psychosocial factors that are
known to influence the immunosurveillance of latent viruses.
As expected, HR-HPV and cervical neoplasia were highly prevalent in our sample. HR-
HPV infection was detected in 78.2% of the study participants, and cervical neoplasia was
present in 81.8% of the participants. Participants in our sample included women who were
asymptomatic, as well as those with advanced HIV disease. Therefore, it is likely that these
results can be generalized to women at any stage of the HIV disease continuum.
Women in this study presented with wide variability in degree of depressive
symptomatology, ranging from endorsing no current depressive symptoms to endorsing
clinically-signifieant depressive symptomatology. It is possible that women with the most severe
depressive symptomatology were not adequately sampled, because they did not present for
routine obstetric and gynecologic care, refused research participation, or did not complete full
study procedures. However, in spite of the challenges of recruiting and retaining participants
with severe depressive symptomatology, 11% of our sample endorsed symptoms suggestive of
clinically significant depression.
Total depressive symptomatology was only marginally associated with cervical neoplasia
in this sample of HIV+ women with HPV infection and there was no relationship between the
cognitive/affective symptoms of depression and cervical neoplasia. Only greater levels of
somatic depressive symptoms were significantly associated with greater odds of cervical
neoplasia, specifically increasing the odds of cervical neoplasia by approximately two-fold. This
finding persisted after controlling for recent negative life event stress, a factor associated with
the progression and/or persistence of cervical neoplasia in our prior research.
This finding is consistent with research suggesting that African Americans, who comprised
the maj ority of our sample, may tend to manifest depression through primarily somatic
symptoms (Das et al., 2006). In addition, it is consistent with the wealth of research
demonstrating that women tend to present frequently with "atypical depression," which includes
somatic symptoms such as weight gain and problems with sleep (Bhatia & Bhatia, 1999). The
results of the current study also appear to be consistent with some published research on somatic
depression and HIV outcomes. Perkins et al. (1995) found that fatigue and insomnia were
associated with dysphoric mood and maj or depressive disorder in HIV+ individuals.
Furthermore, one large-scale, longitudinal study demonstrated that somatic depressive symptoms
were associated with progression to AIDS, progression to HIV-dementia, and shortened survival,
even after controlling for HIV medication use (Farinpour et al., 2003). Taken together, these
findings suggest that somatic depression may be a particularly important marker of depressive
disorders and a correlate of important disease outcomes in HIV.
Caution must be used when interpreting our findings given our modest sample size,
undersampling of severely depressed women, and cross-sectional design, the latter of which
precludes the ability to establish whether somatic depression causes cervical neoplasia or vice-
versa. Of note, the BDI was administered to participants after they had been notified of their
Papanicolaou smear and cervical biopsy results. This was unavoidable given that (a) study
eligibility was based upon these results, and (b) colposcopic examinations were clinically
indicated, and thus it would have been unethical to withhold cytology/histology results from
participants for research purposes. Although this raises some concern that BDI results may be
confounded with CIN-related distress, it should be noted that only participants with no or grade I
(mild) cervical neoplasia were eligible for the study. In addition, approximately four to six
weeks typically elapsed between notification of cytology/histology results and administration of
the BDI, which assessed depressive symptomatology over the prior week only. Finally, an
examination of the BDI and PEAPS-Q scores demonstrated that there was no association
between distress related to the colposcopy and depressive symptoms (p > .05). In concert, these
factors may have restricted the degree of CIN-related distress that could be confounded with
depressive symptomatology. An additional limitation of this study is that several participants did
not have a cervical biopsy performed due the presence of clinical contraindications for biopsy. A
cervical biopsy is necessary to establish a diagnosis of cervical neoplasia, and it is possible that
cervical cytology may have underestimated the degree of cervical neoplasia present among these
Future research should utilize prospective, longitudinal, and/or experimental designs to facilitate
the examination of possible causal mechanisms between depressive symptoms and cervical
neoplasia. For instance, somatic depression may increase odds of cervical neoplasia through
impaired immune functioning. Somatic depression may be associated with a shift in the
production of cytokines from a pattern that promotes cellular immunity (Thl cytokine
production: e.g., interferon-gamma, interleukin-2, tumor necrosis factor-alpha) to one that
promotes primarily humoral immunity (Th2 cytokines production: e.g., interleukin-4,
interleukin-10). This shift has been implicated in the progression of both HPV and HIV (Bais et
al., 2006; Kedzierska & Crowe,2001). Suppression of cellular immunity through a decreased
Thl cytokine response may allow for tumor growth and metastasis to occur (Rankin et al., 2003),
while enhancement of a Th2 cytokine response may promote the survival of cancer cells through
the prevention of programmed cell death ("apoptosis:") (Conticello et al., 2004).
Depression has also been strongly implicated in alterations (increases) in pro-
inflammatory cytokines, including IL-1P, IL-6, and IFN-yI, which are capable of inducing
sickness behaviors, including fatigue, lethargy, muscle and j oint pain, and anorexia (Dantzer,
2006), symptoms that overlap greatly with somatic depressive symptoms. In addition, recent
evidence has indicated that chronic inflammation, and thus an increase in the associated
cytokines, may be involved in carcinogenic processes (Antoni et al., 2006; Balkwill, Charles, &
Mantovani, 2005). Chronic inflammation has also been implicated specifically as a risk factor for
HPV persistence and progression to cervical cancer (Castle, 2004). Thus, bidirectional
relationships between somatic depression and cytokine production, on the one hand, and
cytokine production and cervical neoplasia on the other hand, may account for the present
findings. In the sample used for the current study, greater somatic depressive symptoms were
associated with lower CD4+CD3+ cell counts at study entry (r = -.286, p = .036).
Cognitive/affective depressive symptoms were not associated with CD4+CD3+ cell counts. In
addition, neither somatic nor cognitive/affective depressive symptoms were significantly
associated with HIV viral load, though there was a positive relationship between somatic
depressive symptoms and HIV viral load that approached significance (r = .243, p = .077).
While it is intriguing to consider that cytokine production may mediate the relationship
between somatic depressive symptoms and cervical neoplasia, it is equally possible that this
relationship may be accounted for by the effects of depression on health care behaviors, such as
Papanicolaou smear screening and medication adherence. Therefore, future research should be
guided by a comprehensive model that would allow the testing of (a) multiple mediators of the
relationship between somatic depression and cervical neoplasia, including both cytokine
production and health behaviors, and (b) bidirectional relationships among these variables.
In summary, the findings of the present study suggest that it may be important to assess the
presence and severity of depressive symptoms, most notably somatic depressive symptoms,
among HIV+ women attending gynecologic and obstetric clinics. Ultimately, the identification
and treatment of somatic depression among HIV+ HPV+ women may enhance health-related
quality of life in part via reduction in risk of cervical cancer.
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Stacy Dodd graduated with honors from the University of Michigan in 2005, receiving a
Bachelor of Arts degree in Psychology. During her time at the University of Michigan, she
worked as a research assistant for the Families and Communities Together Coalition on a study
investigating the effects of a group intervention for women and children who had experienced
domestic violence. She also completed an undergraduate honors thesis on the worries of
childhood cancer patients and their mothers and the abilities of each to predict the worries of the
Stacy began attending graduate school at the University of Florida in the department of
Clinical and Health Psychology in August 2005. She is focusing her research on psycho-
oncology, psychneuroimmunology, and women's health. She is currently pursuing her Ph.D. in