Infections by Renibacterium salmoninarum and Nanophyetus salmincola Chapin are associated with reduced growth of juvenile Chinook salmon, Oncorhynchus tshawytscha (Walbaum), in the Northeast Pacific Ocean.

We examined 1454 juvenile Chinook salmon, Oncorhynchus tshawytscha (Walbaum), captured in nearshore waters off the coasts of Washington and Oregon (USA) from 1999 to 2004 for infection by Renibacterium salmoninarum, Nanophyetus salmincola Chapin and skin metacercariae. The prevalence and intensities for each of these infections were established for both yearling and subyearling Chinook salmon. Two metrics of salmon growth, weight residuals and plasma levels of insulin-like growth factor-1, were determined for salmon infected with these pathogens/parasites, both individually and in combination, with uninfected fish used for comparison. Yearling Chinook salmon infected with R. salmoninarum had significantly reduced weight residuals. Chinook salmon infected with skin metacercariae alone did not have significantly reduced growth metrics. Dual infections were not associated with significantly more severe effects on the growth metrics than single infections; the number of triple infections was very low and precluded statistical comparison. Overall, these data suggest that infections by these organisms can be associated with reduced juvenile Chinook salmon growth. Because growth in the first year at sea has been linked to survival for some stocks of Chinook salmon, the infections may therefore play a role in regulating these populations in the Northeast Pacific Ocean.

Growth and condition of juvenile coho salmon Oncorhynchus kisutch relate positively to species richness of trophically transmitted parasites.

The aims of this study were first, to test the hypothesis that metrics of fish growth and condition relate positively to parasite species richness (S(R)) in a salmonid host; second, to identify whether S(R) differs as a function of host origin; third, to identify whether acquisition of parasites through marine v. freshwater trophic interactions was related to growth and condition of juvenile salmonids. To evaluate these questions, species diversity of trophically transmitted parasites in juvenile coho salmon Oncorhynchus kisutch collected off the coast of the Oregon and Washington states, U.S.A. in June 2002 and 2004 were analysed. Fish infected with three or more parasite species scored highest in metrics of growth and condition. Fish originating from the Columbia River basin had lower S(R) than those from the Oregon coast, Washington coast and Puget Sound, WA. Parasites obtained through freshwater or marine trophic interactions were equally important in the relationship between S(R) and ocean growth and condition of juvenile O. kisutch salmon.

Moderating effects of childhood maltreatment on associations between social information processing and adult aggression.

BACKGROUND: Associations between early life maltreatment, social information processing (SIP) and aggression in childhood and adolescence have been widely documented. Few studies have examined the importance of childhood maltreatment independent of SIP in the etiology of adult aggression. Furthermore, moderating effects of childhood maltreatment on the SIP-aggression links have not been explored. METHOD: Hierarchical, multi-level models were fitted to data from n=2752 twins aged 20-55 years from the PennTwins Cohort. Adult aggression was assessed with the Life History of Aggression questionnaire. Childhood maltreatment was measured using the Childhood Trauma Questionnaire. Two aspects of SIP were examined: hostile attribution biases (HAB); negative emotional responses (NER). RESULTS: Childhood maltreatment was positively correlated with adult aggression, independently of HAB and NER. In addition, childhood maltreatment moderated the relationships between both aspects of SIP and adult aggression. Specifically, the relationship between NER and aggression was stronger among individuals with higher levels of childhood maltreatment and NER was not associated with aggression for adults who experienced low levels of childhood maltreatment. Moderating effects of childhood maltreatment on the NER-aggression link were supported for total childhood maltreatment, emotional neglect and emotional abuse. In contrast, HAB was more strongly associated with adult aggression at lower levels of emotional abuse and physical neglect. CONCLUSIONS: The current study provides insight into the mechanisms by which early life experiences influence adult aggression. Our findings suggest that childhood maltreatment may not only lead to increased levels of aggression in adulthood but may also modify the associations between SIP and adult aggression.

Testosterone modifies the effect of APOE genotype on hippocampal volume in middle-aged men.

BACKGROUND: The APOE epsilon4 allele is an established risk factor for Alzheimer disease (AD), yet findings are mixed for how early its effects are manifest. One reason for the mixed results could be the presence of interaction effects with other AD risk factors. Increasing evidence indicates that testosterone may play a significant role in the development of AD. The aim of the present study was to examine the potential interaction of testosterone and APOE genotype with respect to hippocampal volume in middle age. METHODS: Participants were men from the Vietnam Era Twin Study of Aging (n = 375). The mean age was 55.9 years (range 51-59). Between-group comparisons were performed utilizing a hierarchical linear mixed model that adjusted for the nonindependence of twin data. RESULTS: A significant interaction was observed between testosterone and APOE genotype (epsilon4-negative vs epsilon4-positive). Those with both low testosterone (> or =1 SD below the mean) and an epsilon4-positive status had the smallest hippocampal volumes, although comparisons with normal testosterone groups were not significant. However, individuals with low testosterone and epsilon4-negative status had significantly larger hippocampal volumes relative to all other groups. A main effect of APOE genotype on hippocampal volume was observed, but only when the APOE-by-testosterone interaction was present. CONCLUSIONS: These findings demonstrate an interaction effect between testosterone and the APOE epsilon4 allele on hippocampal volume in middle-aged men, and they may suggest 2 low testosterone subgroups. Furthermore, these results allude to potential gene-gene interactions between APOE and either androgen receptor polymorphisms or genes associated with testosterone production.

Avoidant personality disorder symptoms in first-degree relatives of schizophrenia patients predict performance on neurocognitive measures: the UCLA family study.

Whether avoidant personality disorder symptoms are related to neurocognitive impairments that aggregate in relatives of schizophrenics is unknown. We report the relationship between avoidant personality disorder symptoms and neurocognitive performance in the first-degree relatives of probands with schizophrenia. 367 first-degree relatives of probands with schizophrenia and 245 relatives of community controls were interviewed for the presence of avoidant personality symptoms and symptoms of paranoid and schizotypal personality disorders and administered neurocognitive measures. Relationships between neurocognitive measures and avoidant symptoms were analyzed using linear mixed models. Avoidant dimensional scores predicted performance on the span of apprehension (SPAN), 3-7 Continuous Performance Test (3-7 CPT), and Trail Making Test (TMT-B) in schizophrenia relatives. These relationships remained significant on the SPAN even after adjustment for paranoid or schizotypal dimensional scores and on the TMT-B after adjustment for paranoid dimensional scores. Moreover, in a second set of analyses comparing schizophrenia relatives to controls there were significant or trending differences in the degree of the relationship between avoidant symptoms and each of these neurocognitive measures even after adjustments for paranoid and schizotypal dimensional scores. The substantial correlation between avoidant and schizotypal symptoms suggests that these personality disorders are not independent. Avoidant and in some cases schizotypal dimensional scores are significant predictors of variability in these neurocognitive measures. In all analyses, higher levels of avoidant symptoms were associated with worse performance on the neurocognitive measures in relatives of schizophrenia probands. These results support the hypothesis that avoidant personality disorder may be a schizophrenia spectrum phenotype.

Apolipoprotein E genotype and memory in the sixth decade of life.

BACKGROUND: Virtually all adult studies of APOE genotypes and cognition have included individuals over 60. In older adults, epsilon 4 carriers may manifest greater cognitive asymmetries than non-epsilon 4 carriers even in the absence of overall mean differences. General cognitive ability may also be affected by aging and APOE genotype, but most studies have inadequately addressed this potential confound. The goals of this study were to examine, in middle age, the relationship of APOE genotype with episodic memory and verbal-visuospatial episodic memory asymmetries, after accounting for prior general cognitive ability. METHOD: We compared epsilon 4+ and epsilon 4- individuals in 626 male twins in their 50s. We examined verbal and visuospatial episodic memory and verbal-visual asymmetry scores after adjusting for cognitive ability at age 20. Analyses corrected for correlations between twin pair members. RESULTS: Compared with epsilon 4- individuals, epsilon 4 carriers performed significantly more poorly on verbal, but not visuospatial memory, manifested significantly greater cognitive asymmetry, and also had significantly more concerns about memory. At age 20, epsilon 4 carriers had higher general cognitive ability than epsilon 4- individuals, and current memory differences were enhanced after adjusting for age 20 cognitive ability. CONCLUSIONS: Small, but significant, APOE-epsilon 4-related memory deficits appear in the sixth decade of life in individuals who show no signs of preclinical dementia. The results partially support studies of older adults that suggest that increased cognitive asymmetries reflect risk for dementia and are associated with the APOE-epsilon 4 genotype. The results also highlight the potential problems of not having accurate data on prior cognitive ability.

Avoidant personality disorder is a separable schizophrenia-spectrum personality disorder even when controlling for the presence of paranoid and schizotypal personality disorders The UCLA family study.

It is unresolved whether avoidant personality disorder (APD) is an independent schizophrenia (Sz)-spectrum personality disorder (PD). Some studies find APD and social anxiety symptoms (Sxs) to be separable dimensions of psychopathology in relatives (Rels) of schizophrenics while other studies find avoidant Sxs to be correlated with schizotypal and paranoid Sxs. Rates of APD among first-degree Rels of Sz probands, attention-deficit/hyperactivity disorder (ADHD) probands, and community control (CC) probands were examined. Further analyses examined rates when controlling for the presence of schizotypal (SPD) and paranoid (PPD) personality disorders, differences in APD Sxs between relative groups, and whether APD in Rels of Szs reflects a near miss for another Sz-spectrum PD. Three hundred sixty-two first-degree Rels of Sz probands, 201 relatives of ADHD probands, and 245 Rels of CC probands were interviewed for the presence of DSM-III-R Axis I and II disorders. Diagnoses, integrating family history, interview information, and medical records, were determined. APD occurred more frequently in Rels of Sz probands compared to CC probands (p<0.001) and also when controlling for SPD and PPD (p<0.005). Two Sxs of APD were most characteristic of the Rels of Sz probands: "avoids social or occupational activities..." and "exaggerates the potential difficulties..." 65% of the Rels of Sz probands who had diagnoses of APD were more than one criterion short of a DSM-III-R diagnosis of either SPD or PPD. This indicates that APD is a separate Sz-spectrum disorder, and not merely a sub-clinical form of SPD or PPD.

Illicit drug use and abuse/dependence: modeling of two-stage variables using the CCC approach.

Drug use and abuse/dependence are stages of a complex drug habit. Most genetically informative models that are fit to twin data examine drug use and abuse/dependence independent of each other. This poses an interesting question: for a multistage process, how can we partition the factors influencing each stage specifically from the factors that are common to both stages? We used a causal-common-contingent (CCC) model to partition the common and specific influences on drug use and abuse/dependence. Data on use and abuse/dependence of cannabis, cocaine, sedatives, stimulants and any illicit drug was obtained from male and female twin pairs. CCC models were tested individually for each sex and in a sex-equal model. Our results suggest that there is evidence for additive genetic, shared environmental and unique environmental influences that are common to illicit drug use and abuse/dependence. Furthermore, we found substantial evidence for factors that were specific to abuse/dependence. Finally, sexes could be equated for all illicit drugs. The findings of this study emphasize the need for models that can partition the sources of individual differences into common and stage-specific influences.

A twin study of personality and illicit drug use and abuse/dependence.

Although personality measures such as neuroticism (N), extraversion (E) and novelty-seeking (NS) are associated with the use and abuse/dependence of illicit drugs, little is known about the degree to which these associations are due to genetic or environmental factors. The goal of this analysis was to estimate the extent of genetic and environmental overlap between three dimensions of personality (N, E and NS) and illicit psychoactive substance use and abuse/dependence. Using data from adult male and female twins from the Mid-Atlantic Twin Registry, we used the structural equation modeling package Mx to perform bivariate Cholesky decompositions for personality measures of N, E and NS, individually with cannabis, cocaine, sedatives, stimulants and hallucinogens. This was done separately for use and for a polychotomous diagnosis of abuse and/or dependence. Sex differences were tested. The phenotypic relationship between personality and use and abuse/dependence of illicit drugs were moderate and most of the covariance was explained by genetic factors. Sexes could be equated for N and E but not for NS. For NS, use and abuse/dependence of illicit drugs showed greater phenotypic and genetic overlap in males than females. Of the personality measures, NS and illicit drug use and abuse/dependence were most closely related. NS was most closely related to cannabis use while N showed significant genetic overlap with sedative use. NS in males appears to be a good indicator of risk for cannabis use. This result may be useful for candidate gene studies.

Does the level of family dysfunction moderate the impact of genetic factors on the personality trait of neuroticism?

BACKGROUND: While the family environment can directly influence later risk for psychopathology, dysfunction in the family of origin may also moderate the impact of genetic factors on liability for psychiatric disorders. Can a similar pattern be seen for the personality trait of Neuroticism (N)-which is a risk factor for many psychiatric conditions? METHOD: Our sample of 957 complete female-female twin pairs from a population-based register had measures of self-reported N and multiple reporters (twin, co-twin, mother, father) for family dysfunction (FD). Statistical analysis was conducted by traditional regression analysis and a moderator structural equation twin model operationalized in the computer program Mx. RESULTS: Dividing the sample into quartiles based on increasing levels of FD, the mean of N increased substantially while correlations of N in monozygotic (MZ) and dizygotic (DZ) twins were relatively constant. Regression analyses did not suggest greater twin resemblance for N with increasing levels of FD. The best-fit structural equation model was the standard un-moderated model in which the proportion of variance in N due to genetic (39%) and unique environmental effects (61%) remained constant across values of FD. CONCLUSIONS: Although a false-negative result due to limited power cannot be excluded, these analyses do not support the hypothesis that FD moderates the impact of genetic factors on levels of N.

A twin study of sex differences in social support.

BACKGROUND: Social support may reduce the risk of psychiatric illness. Though perceived as an environmental measure, genetic factors may influence levels of social support. A relationship between social roles and personality with social support suggests possible sex effects on the sources of individual differences in social support. METHOD: We used the responses of MZ and DZ same and opposite sex twins to 16 questions regarding their social life. Six factors--friend support, relative support, friend problem, relative problem, confidants and social integration were used for structural equation modelling. Factor derived scales were analysed for genetic, shared and unique environmental influences. Quantitative and qualitative gender differences were analysed using the software package Mx. RESULTS: Except for relative support and confidants, no qualitative sex differences were seen. Genetic and individual specific environmental influences accounted for the variance for friend support, friend problems, relative problems and social integration and no quantitative gender differences were seen. For relative support genetic factors were detected in females but not males, while for confidants, the shared environment was important in females but not males. CONCLUSIONS: Except for relative support in males, genetic factors influence variation in all dimensions of social support. Shared environmental factors influence relative support and relative problems in both sexes. Sex differences were detected for confidants and relative support.

Sex differences in genetic and environmental risk factors for irrational fears and phobias.

BACKGROUND: For irrational fears and their associated phobias, epidemiological studies suggest sex differences in prevalence and twin studies report significant genetic effects. How does sex impact on the familial transmission of liability to fears and phobias? METHODS: In personal interviews with over 3000 complete pairs (of whom 1058 were opposite-sex dizygotic pairs), ascertained from a population-based registry, we assessed the lifetime prevalence of five phobias and their associated irrational fears analysed using a multiple threshold model. Twin resemblance was assessed by polychoric correlations and biometrical model-fitting incorporating sex-specific effects. RESULTS: For agoraphobia, situational and blood/injury fear/phobia, the best fit model suggested equal heritability in males and females and genetic correlations between the sexes of less than +0.50. For animal fear/phobias by contrast, the best fit model suggested equal heritability in males and females and a genetic correlation of unity. No evidence was found for an impact of family environment on liability to these fears or phobias. For social phobias, twin resemblance in males was explained by genetic factors and in females by familial-environmental factors. CONCLUSION: The impact of sex on genetic risk may differ meaningfully across phobia subtypes. Sex-specific genetic risk factors may exist for agoraphobia, social, situational and blood-injury phobias but not for animal fear/phobia. These results should be interpreted in the context of the limited power of twin studies, even with large sample sizes, to resolve sex-specific genetic effects.

Genetic and environmental influences on juvenile antisocial behaviour assessed on two occasions.

BACKGROUND: There is conflicting evidence concerning the magnitude of genetic and shared environmental influences on juvenile antisocial behaviour (AB). The use of more than one assessment of AB may yield more accurate estimates of these influences. METHODS: Retrospective reports of antisocial behaviour prior to age 18 were obtained on two occasions from a population-based sample of 3522 adult males from male-male twin pairs: phone interviews (wave 1) and self-report questionnaires obtained 19 months later (wave 2). Structural equation modelling estimated the genetic and environmental influences on reliably-measured AB. Factors related to participation of co-twin at wave 1, attrition between waves 1 and 2, and reliability of wave 1 and wave 2 assessments were also investigated. RESULTS: Twin analyses revealed that genetic, shared environmental, and non-shared environmental influences accounted for approximately 33% (95% CI = 9-57%), 31% (95% CI = 10-51%) and 36% (95% CI = 29-44%) of the variance of reliably measured AB, respectively. We also found significant occasion-specific genetic influences on wave 1 AB. Wave 1 AB did not predict wave 1 participation of co-twin or attrition, but was related to reliability. Co-twins of MZ twins and younger twins were more likely to participate at wave 1; attrition was predicted by being a DZ twin, lack of initial participation of co-twin, fewer years of education, and fewer children. Being older, being unmarried, and having less psychopathology were associated with greater reliability. CONCLUSIONS: When measurement error is taken into account, both genetic and shared environmental factors are significant influences on juvenile AB, accounting for approximately one-third of variation. The origin of the specific genetic influences on wave 1 AB is unclear, but may be due to factors related to measurement.

Cohort differences in genetic and environmental influences on retrospective reports of conduct disorder among adult male twins.

BACKGROUND: Rates of child and adolescent conduct disorder (CD) have increased steadily over the past several decades. What is not known is whether the underlying genetic and environmental influences on individual differences in CD have also changed. METHODS: Retrospective reports of antisocial behaviour prior to age 18 were obtained from a population-based sample of 2769 adult males from male-male twin pairs born between 1940 and 1974. Using a summary score of number of CD symptoms, structural equation modelling was used to investigate whether mean level and variation in CD increased with more recent cohorts, and whether any increase in variance could be explained by familial or non-familial factors. RESULTS: Both mean level CD symptoms and variation were increased in more recent cohorts. Model fitting indicated that the primary increase in variance was due to familial factors, most notably, an increase in the shared environmental influences on CD, from 0.01 (95 % CI = 0.00; 0.27) to 0.30 (95 % Cl = 0.01; 0-44). Heritability estimates remained largely unchanged, although an increase in genetic factors could not be ruled out. CONCLUSIONS: Secular changes in sociodemographic factors responsible for increasing rates of CD may also account for the greater magnitude of shared environmental influences on variation in CD found among more recent cohorts.

Genetic and environmental influences on vocabulary IQ: parental education level as moderator.

This article examines how parental education level moderates the genetic and environmental contributions to variation in verbal IQ. Data are from 1909 non-Hispanic Whites and African American sibling pairs from the National Longitudinal Study of Adolescent Health, which obtained nationally-based samples of identical (MZ) twins, fraternal (DZ) twins, full and half siblings, cousins (in the same household), and biologically unrelated siblings. In the whole sample, the variance estimate for heritability (h2 = .57, SE = .08) was greater than that for shared environment (c2 = .13, SE = .04). Both heritability and the shared environmental estimate were moderated, however, by level of parental education. Specifically, among more highly educated families, the average h2 = .74 (SE = .10) and the average c2 = .00 (SE = .05). Conversely, among less well-educated families, heritability decreased and shared environmental influences increased, yielding similar proportions of variance explained by genetic and environmental factors, average h2 = .26 (SE = .15), and average c2 = .23 (SE = .07).

Genetic and environmental influences on the relationships between family connectedness, school connectedness, and adolescent depressed mood: sex differences.

This study investigated (a) genetic and environmental contributions to the relationship between family and school environment and depressed mood and (b) potential sex differences in genetic and environmental contributions to both variation in and covariation between family connectedness, school connectedness, and adolescent depressed mood. Data are from 2,302 adolescent sibling pairs (mean age = 16 years) who were part of the National Longitudinal Study of Adolescent Health. Although genetic factors appeared to be important overall, model-fitting analyses revealed that the best-fitting model was a model that allowed for different parameters for male and female adolescents. Genetic contributions to variation in all 3 variables were greater among female adolescents than male adolescents, especially for depressed mood. Genetic factors also contributed to the correlations between family and school environment and adolescent depressed mood, although, again, these factors were stronger for female than for male adolescents.

Genetic and shared environmental influences on adolescent BMI: interactions with race and sex.

The present study uses a behavioral genetic design to investigate the genetic and environmental influences on variation in adolescent body mass index (BMI) and to determine whether the relative influences of genetic and environmental factors on variation in BMI are similar across racial groups and sexes. Data for the present study come from the National Longitudinal Study on Adolescent Health (Add Health), a large, nationally representative study of adolescent health and health-related behaviors. The Add Health sample contains a subset of sibling pairs that differs in levels of genetic relatedness, making it well suited for behavioral genetics analyses. The present study examines whether genetic and environmental influences on adolescent BMI are the same for males and females and for Black and White adolescents. Results indicate that genetic factors contribute substantially to individual differences in adolescent BMI, explaining between 45 and 85% of the variance in BMI. Furthermore, based on an analysis of opposite-sex sibling pairs, the genes that influence variation in adolescent BMI are similar for males and females. However, the relative importance of genetic and environmental influences on variation in BMI differs for males and females and for Blacks and Whites. Although parameter estimates could be constrained to be equal for Black and White males, they could not be constrained to be equal for Black and White females. Moreover, the best-fitting model for Black females was an ADE model, for White females it was an ACE model, and for males it was an AE model. Thus, shared environmental influences are significant for White female adolescents, but not for Black females or males. Likewise, nonadditive genetic influences are indicated for Black females, but not for White females or males. Implications of these results are discussed.

A study of antibody and T cell recognition of rhoptry-associated protein-1 (RAP-1) and RAP-2 recombinant proteins and peptides of Plasmodium falciparum in migrants and residents of the state of Rondonia, Brazil.

Humoral and cellular responses were examined among natives and migrants in an area of the Amazon region of Brazil. Rhoptry-associated protein-1 (RAP-1) and RAP-2 expressed in Escherichia coli expression systems, a peptide corresponding to the epitope bound by inhibitory anti-RAP-1 antibodies, and four other RAP-1 and RAP-2 synthetic peptides were used in these studies. Plasma from the native population had greater IgG reactivity to the N-terminal third of RAP-1 than the migrant population; both populations had low levels of IgM to this region of RAP-1. The IgG reactivity to RAP-2 and to the C-terminal third of RAP-1, as well as for all the peptides, including the peptide from the inhibitory domain, were low or absent in both populations. In contrast, there were a high number of subjects with an IgM response to the peptides. Cellular responses were measured by proliferation of peripheral blood mononuclear cells (PBMC) and, in some subjects, by reverse transcription-polymerase chain reaction for interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-4, and IL-10. Proliferation of PBMC was low when stimulated by recombinant proteins, peptides, or parasite lysate. Both RAP-1 and RAP-2 stimulated cytokine production by donor T cells; IL-2, IL-4, and IFN-gamma RNA transcripts were observed in response to recombinant proteins and parasite lysate, but with no uniform trends. From the observed antibody responses, RAP-1 appears to be more immunogenic than RAP-2.

Analysis of inhibitory epitopes in the Plasmodium falciparum rhoptry protein RAP-1 including identification of a second inhibitory epitope.

Immune responses to Plasmodium falciparum rhoptry-associated protein 1 (RAP-1), RAP-2, and RAP-3 appear to contribute to protection against infection by this human malarial parasite. This conclusion is suggested by results of monkey immunization trials and of cell culture studies showing antibody-dependent inhibition of erythrocyte invasion. In the present study, splenectomized owl monkeys were infected with P. falciparum in order to monitor anti-RAP-1 antibody production as antiparasite immunity developed. The monkeys responded to a primary infection with the production of antibodies to a fragment of RAP-1 containing amino acids 1 to 294 (RAP-1(1-294)). After drug cure and reinfection, the monkeys had a prolonged prepatent period, indicating they had already developed partial immunity to the parasite. Sera from these animals showed major increases in anti-RAP-1(1-294) antibodies. In contrast, only low levels of antibodies to inhibitory B-cell epitope 1 (iB-1), an inhibitory epitope in RAP-1(1-294) with the sequence N200TLTPLEELYPT211, was observed after the initial parasite infection, and the anti-iB-1 antibodies were not readily boosted upon reinfection. These results suggest that iB-1 is an immunogenic but not immunodominant epitope and that anti-iB-1 antibodies do not substantially contribute to early stages of naturally acquired immunity in the owl monkey model. To identify additional epitopes bound by inhibitory antibodies, mouse monoclonal antibodies were produced with a recombinant fusion protein containing RAP-1(1-294). Monoclonal antibody 1D6 inhibited parasite invasion of erythrocytes in vitro. 1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2. iB-2, like iB-1, is found near the amino terminus of p67, a RAP-1 processing product thought to be involved in merozoite invasion of erythrocytes. Since anti-iB-1 antibodies were not readily produced during parasite infection, it may be desirable to direct antibody responses to particular epitopes in RAP-1, such as iB-1 and iB-2.