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PubMed1997

Schistosoma japonicum infection in the pig: the effect of a patent primary infection on a challenge infection.

The response of pigs to a challenge infection of Schistosoma japonicum following a primary infection was assessed using parasitological parameters and eosinophil counts. Twenty-five Danish Landrace/Yorkshire/Duroc crossbred pigs were divided into four groups. Group A (n = 10) received a primary infection, group B (n = 5) received both a primary and challenge infection, group C (n = 5) received a challenge control infection and group D (n = 5) received no infection serving as helminth-free controls. A dose of 850 cercariae was administered by intramuscular injection at the primary infection (week 0) and challenge infection (week 12). The pigs were perfused at week 21, except for half of the group A pigs which were slaughtered at week 12. Challenge infection did not result in higher worm burdens or tissue egg counts in group B than group A at week 21 and mature/immature worm ratios were similar for the two groups. In addition, no increases in faecal egg counts or eosinophil counts were observed in group B after challenge infection. The results indicate that pigs are able to mount a very rapid and effective response to reinfection with S. japonicum following a patent primary infection resulting in prevention of establishment of challenge infection schistosomes. An anti-worm effect appears to be the main feature of this regulatory host response.

Animals↗
PubMed2002

Failure to spread bovine virus diarrhoea virus infection from primarily infected calves despite concurrent infection with bovine coronavirus.

Previous reports on the spread of bovine virus diarrhoea virus (BVDV) from animals primarily infected with the agent are contradictory. In this study, the possibility of transmission of BVDV from calves simultaneously subjected to acute BVDV and bovine coronavirus (BCV) infection was investigated. Ten calves were inoculated intranasally with BVDV Type 1. Each of the 10 calves was then randomly allocated to one of two groups. In each group there were four additional calves, resulting in five infected and four susceptible calves per group. Virulent BCV was actively introduced in one of the groups by means of a transmitter calf. Two calves, susceptible to both BVDV and BCV, were kept in a separate group, as controls. All ten calves actively inoculated with BVDV became infected as shown by seroconversions, and six of them also shed the virus in nasal secretions. However, none of the other eight calves in the two groups (four in each) seroconverted to this agent. In contrast, it proved impossible to prevent the spread of BCV infection between the experimental groups and consequently all 20 study calves became infected with the virus. Following infection, BCV was detected in nasal secretions and in faeces of the calves and, after three weeks in the study, all had seroconverted to this virus. All calves, including the controls, showed at least one of the following clinical signs during days 3-15 after the trial started: fever (> or =40 degrees C), depressed general condition, diarrhoea, and cough. The study showed that BVDV primarily infected cattle, even when co-infected with an enteric and respiratory pathogen, are inefficient transmitters of BVDV. This finding supports the principle of the Scandinavian BVDV control programmes that elimination of BVDV infection from cattle populations can be achieved by identifying and removing persistently infected (PI) animals, i.e. that long-term circulation of the virus without the presence of PI animals is highly unlikely.

Acute Disease↗
PubMed1982

The development of clinical tuberculosis following infection with tubercle bacilli. 1. A theoretical model for the development of clinical tuberculosis following infection, linking from data on the risk of tuberculous infection and the incidence of clinical tuberculosis in the Netherlands.

Information on the risk of tuberculous infection in the Netherlands has been linked with information on the incidence of tuberculosis, in an attempt to estimate the risks of developing the disease following infection or reinfection. It was postulated that: (a) those with a recent primary infection had a characteristic risk of developing progressive primary tuberculosis; (b) those with a distant (i.e. not recent) primary infection and a recent reinfection had a characteristic risk of developing exogenous tuberculosis; and (c) those with a distant primary infection but no recent reinfection had a characteristic risk of developing endogenous tuberculosis. The information on the risk of tuberculous infection was used to estimate the size of the population in each of these infection classes for different age-groups and calendar years in the Netherlands. Using multiple regression to link these population figures with the information on tuberculosis incidence in the same age group and calendar year, it was possible to estimate the above risks of developing tuberculosis. For Netherlands males aged 15-69 years during the period 1951-70 the three risks of developing pulmonary tuberculosis were estimated to be: (a) 5.06 per cent annually (for 5 years) following primary infection; (b) 1.91 per cent annually (for 5 years) following reinfection; (c) 0.0253 per cent annually, after the first 5 years following primary infection, in the absence of reinfection. The corresponding (and significantly different) estimated annual risks of development of pulmonary tuberculosis for females were 5.85, 1.10 and 0.0020 per cent respectively. From these risks, it may be estimated that the degree of protection conferred by a distant primary infection, against pulmonary tuberculosis arising from a recent reinfection, was 63 per cent for males and 81 per cent for females. The estimated relative proportions of cases of progressive primary, exogenous and endogenous tuberculosis varied considerably with age and calendar year. Progressive primary tuberculosis was dominant at the younger ages, exogenous and endogenous tuberculosis at older ages. At these older ages, the great majority of cases in the Netherlands in the early 1950s appeared to be exogenous in origin, but by 1970, with the decrease in the risk of infection, the exogenous contribution had dwindled substantially, especially among males.

Adolescent↗
PubMed2001

Infection after laparoscopic cholecystectomy: effect of infected bile and infected gallbladder wall.

OBJECTIVE: To assess the incidence of infected bile and gallbladder wall infection at the time of laparoscopic cholecystectomy, and find out if they influenced the rate of postoperative infective complications. DESIGN: Prospective study. SETTING: District hospital, Kuwait. SUBJECTS: All 279 patients who had their gallbladders removed laparoscopically for gallbladder disease between September 1995 and August 1998. INTERVENTIONS: Samples of bile and gallbladder wall were taken from all patients and cultured separately for aerobic and anaerobic bacteria. Patients with complicated gallbladder disease (n = 80) were given preoperative therapeutic antibiotics for five days (cephalosporin plus metronidazole), and other high-risk patients (n = 138) were given prophylactic ceftriaxone either 1 g x 3 starting at induction of anaesthesia (n = 42), or a single dose at induction (n = 96). MAIN OUTCOME MEASURES: Incidence of infected cultures, and infective morbidity. RESULTS: 26 specimens of bile (9%) and 56 specimens of gallbladder wall (20%) were infected. Two patients in whom neither specimen had shown any growth developed minor infections at the umbilical port. No patient in whom either specimen was infected developed an infective complication. CONCLUSIONS: The overall rate of infective complications was negligible, and did not correlate with the presence of bacteria in the bile or gallbladder wall. This is probably a reflection of our aggressive antibiotic regimen in the management of high-risk patients.

Adolescent↗
PubMed1967

Experimental transmission of influenza virus infection in mice. 3. Differing effects of immunity induced by infection and by inactivated influenza virus vaccine on transmission of infection.

Immunization of mice by infection or intraperitoneal injection with homotypic A(2), heterotypic A(0), or recombinant A(0)A(2) virus have differing effects on transmission of influenza A(2) virus infection. Immunization by infection with A(2) virus resulted in refractoriness to reinfection either by artificial aerosols or by exposure to infected cage-mates. Immunization by inoculation with inactivated A(2) virus vaccine resulted in a decreased susceptibility to transmitted infection in immunized contacts, but following A(2) virus challenge, transmission of infection by immunized infectors was not altered. Immunization by infection with influenza A(0) virus or recombinant A(0)A(2) virus resulted in a decreased susceptibility to transmitted A(2) virus infection in immunized contacts, and to decreased transmission after A(2) virus infection in immunized infector mice. These differing effects on transmission of infection are attributed to differences in specific local immunologic responses following the various immunization procedures.

Animals↗
PubMed1995

Infection of central nervous system cells by ecotropic murine leukemia virus in C58 and AKR mice and in in utero-infected CE/J mice predisposes mice to paralytic infection by lactate dehydrogenase-elevating virus.

Certain mouse strains, such as AKR and C58, which possess N-tropic, ecotropic murine leukemia virus (MuLV) proviruses and are homozygous at the Fv-1n locus are specifically susceptible to paralytic infection (age-dependent poliomyelitis [ADPM]) by lactate dehydrogenase-elevating virus (LDV). Our results provide an explanation for this genetic linkage and directly prove that ecotropic MuLV infection of spinal cord cells is responsible for rendering anterior horn neurons susceptible to cytocidal LDV infection, which is the cause of the paralytic disease. Northern (RNA) blot hybridization of total tissue RNA and in situ hybridization of tissue sections demonstrated that only mice harboring central nervous system (CNS) cells that expressed ecotropic MuLV were susceptible to ADPM. Our evidence indicates that the ecotropic MuLV RNA is transcribed in CNS cells from ecotropic MuLV proviruses that have been acquired by infection with exogenous ecotropic MuLV, probably during embryogenesis, the time when germ line proviruses in AKR and C58 mice first become activated. In young mice, MuLV RNA-containing cells were found exclusively in white-matter tracts and therefore were glial cells. An increase in the ADPM susceptibility of the mice with advancing age correlated with the presence of an increased number of ecotropic MuLV RNA-containing cells in the spinal cords which, in turn, correlated with an increase in the number of unmethylated proviruses in the DNA extracted from spinal cords. Studies with AKXD recombinant inbred strains showed that possession of a single replication-competent ecotropic MuLV provirus (emv-11) by Fv-1n/n mice was sufficient to result in ecotropic MuLV infection of CNS cells and ADPM susceptibility. In contrast, no ecotropic MuLV RNA-positive cells were present in the CNSs of mice carrying defective ecotropic MuLV proviruses (emv-3 or emv-13) or in which ecotropic MuLV replication was blocked by the Fv-1n/b or Fv-1b/b phenotype. Such mice were resistant to paralytic LDV infection. In utero infection of CE/J mice, which are devoid of any endogenous ecotropic MuLVs, with the infectious clone of emv-11 (AKR-623) resulted in the infection of CNS cells, and the mice became ADPM susceptible, whereas littermates that had not become infected with ecotropic MuLV remained ADPM resistant.

Animals↗
PubMed1981

Infection of Aedes aegypti with Brugia pahangi administered by enema: results of quantitative infection and loss of infective larvae during blood feeding.

A technique for infecting mosquitoes with known numbers of Brugia pahangi microfilariae by enema is described. Virtually all mosquitoes receiving three microfilariae or more by this route contained infective larvae 10 days later. Within a range of 1 to 40 microfilariae, numbers of infective larvae recovered (Y) were related to the numbers of microfilariae administered (X) by the equation log10Y=0.04 + 0.84 log10X. Mosquitoes feeding on sugar for up to 20 days did not lose a significant number of infective larvae. A blood meal 10 days after infection reduced the proportion of females still infected, as well as the number of worms remaining in those still infected. A second blood meal on day 17 after infection only reduced the proportion of mosquitoes still infected. Adults reared on a low larval diet were less susceptible to infection, and a refractory mosquito strain did not support the development of third-stage larvae. Filarial worms had no effect on mosquito mortality until more than 30 microfilariae were administered.

Aedes↗
PubMed1985

Vaccinia virus antigens on the plasma membrane of infected cells. I. Viral antigens transferred from infecting virus particles and synthesized after infection.

SDS-polyacrylamide gel electrophoretic analysis of plasma membranes prepared from L cells infected with radioiodinated vaccinia virus particles showed that at 2.0 hr postinfection, 125I-labeled virion polypeptides with molecular weights of 58K-60K, 32K-34K, 17K, and 12K-14K were associated with infected cell plasma membranes. By 4 hr postinfection, only the 32- to 34-kDa polypeptide, derived from infecting virus particles, could be detected on infected cell surfaces. A variety of techniques were applied to analyzing purified plasma cell membranes to define the viral antigens expressed on cell surfaces after infection, including (a) surface radioiodination of infected cells; (b) immune or Western blotting; (c) specific immunoprecipitation of viral proteins present in nonionic detergent extracts of membranes purified from [35S]methionine-labeled, virus-infected cells. It was determined that vaccinia virus-specified polypeptides with molecular weights of 78K-82K, 65K, 50K, 42K-45K, 35K-37K, 32K-34K, 30K, 20K, and 17K-18K were expressed by 3 hr postadsorption, on the plasma membranes of infected cells and were accessible to binding by exogenous antiviral antibodies. Viral antigens with molecular weights similar to those expressed on cell surfaces were secreted or shed from infected cells and could be detected in the medium harvested from virus-infected mouse L-cell cultures.

Adsorption↗
PubMed1999

Infection with Toxoplasma gondii RH and Prugniaud strains in mice, rats and nude rats: kinetics of infection in blood and tissues related to pathology in acute and chronic infection.

Since mice and rats are the most studied models of experimental toxoplasmosis, the aim of this work was to analyze the outcome of Toxoplasma infection in mice, rats and congenitally athymic nude rats; for this purpose, the parasitic load in different organs and the anatomic-pathological characteristics of infection were investigated in these animals. The data obtained after infection with two different strains and stages of Toxoplasma gondii (RH tachyzoites and Prugniaud cysts) concerned the following organs: brain, mesenteric lymph nodes, blood, spleen, heart, lungs, diaphragm and liver. In Fischer rats, the infection with either the Prugniaud or the RH strains displayed similar characteristics: after a peak in the parasite load, a complete disappearance of parasites was observed, except in the brain of Prugniaud strain-infected rats where toxoplasmas were evidenced throughout the experiment. In OF1 mice, where infection by the RH tachyzoites was lethal, infection with the Prugniaud strain led to survival; the parasitic burden peaked in the different organs and was then undetectable, except in the brain where toxoplasmas were still present during the chronic phase. Like mice, nude rats did not survive to the RH infection. Interestingly, for all the animals the observed histopathological changes in the infected organs, although more or less obvious in the acute phase, were not very severe in almost all cases. For instance, mice, although more susceptible to infection than rats, did not present more severe lesions. They consisted in a discrete inflammation with some focal areas of necrosis in some organs such as brain, liver and heart. Our results support the assumption that rats and nude rats constitute interesting experimental models relevant to either human acute toxoplasmosis, chronic toxoplasmosis, or disseminated toxoplasmosis in AIDS patients.

Acute Disease↗
PubMed1999

Ovine lentivirus-infected macrophages mediate productive infection in cell types that are not susceptible to infection with cell-free virus.

Ovine lentiviruses and caprine arthritis-encephalitis virus (CAEV) are prototypic lentiviruses that replicate predominantly in macrophages of infected animals. In situ hybridization of pathologically affected tissues from diseased animals has shown that viral RNA exists in permissive macrophages as well as in non-macrophage cell types that do not support productive virus replication. These findings raise questions about the cellular tropism of these viruses in vivo and how this may relate to their pathogenesis and the establishment of persistent infections. In this study, the susceptibility of macrophages and fibro-epithelial cells derived from goat synovial membrane (GSM) to infection by 14 North American ovine lentivirus strains was examined. All 14 strains were macrophage-tropic, as indicated by expression of viral proteins and by fusion and development of syncytial cytopathic effects following co-culture of infected macrophages with GSM cells. In contrast, neither viral DNA nor viral proteins was detected in GSM cells inoculated with cell-free virus from nine of the 14 strains. Specific virus proteins were immunoprecipitated from restrictive GSM cells following culture with infected macrophages and serial passage of GSM cells to remove the macrophages. The lack of infection of GSM cells by cell-free virus from some ovine lentivirus field strains was circumvented by cell-associated virus infection from infected macrophages to GSM cells following cell-to-cell contact. This strategy could be one of the mechanisms involved in the escape from immune surveillance and establishment of persistent infection in infected animals.

Animals↗
PubMed2004

Fungal infection but not type of bacterial infection is associated with a high mortality in primary and secondary infected pancreatic necrosis.

INTRODUCTION: Knowledge of microbiology in the prognosis of patients with necrotizing pancreatitis is incomplete. AIM: This study compared outcomes based on primary and secondary infection after surgery for pancreatic necrosis. METHOD: From a limited prospective database of pancreatic necrosectomy, a retrospective case note review was performed (October 1996 to April 2003). RESULTS: 55 of 73 patients had infected pancreatic necrosis at the first necrosectomy. 25 of 47 patients had resistant bacteria to prophylactic antibiotics (n = 21) or did not receive prophylactic antibiotics (n = 4), but this was not associated with a higher mortality (9 of 25) compared to those with sensitive organisms (4 of 22). Patients with fungal infection (n = 6) had a higher initial median (95% CI) APACHE II score compared to those without (11 (9-13) verus 8.5 (7-10), p = 0.027). Five of six patients with fungal infection died compared to 13 of 47 who did not (p = 0.014). With the inclusion of secondary infections 21 (32%) of 66 patients had fungal infection with 10 (48%) deaths compared to 11 (24%) of 45 patients without fungal infection (p = 0.047). CONCLUSION: Whether associated with primary or secondary infected pancreatic necrosis, fungal but not bacterial infection was associated with a high mortality.

Bacterial Infections↗
PubMed1987

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. III. Experimental transmission of infection and derivation of virus-free progeny from previously infected dams.

The incidence and duration of transmission of infection with ectromelia virus strain NIH-79 was tested in innately resistant (C57BL/6) and innately susceptible (BALB/c) inbred mice. Transmission by C57BL/6 index mice occurred through 3 weeks and by BALB/c index mice through 4 weeks, although the duration of infection in individual index mice was often shorter. Soiled caging that previously housed infected mice was inconsistently infectious. Transmission was high in cages where infected mice died and were cannibalized by cagemates, but was low to moderate in cages where there was no cannibalism. Infected mice that were bred 6 weeks after they were infected, delivered virus-free progeny and did not transmit infection to their non-immune breeding partners. Sentinel mice housed in the room with experimentally infected mice were seronegative for antibody to ectromelia virus and to other murine viruses. These results support the view that infection with NIH-79 virus is typically short-lived. They also indicate that breeding of recovered mice can save valuable colonies that have been exposed to ectromelia virus.

Animals↗
PubMed2005

Reinfections, persistent infections, and new infections after general population screening for Chlamydia trachomatis infection in the Netherlands.

OBJECTIVES: The objectives of this study were to determine the rate of new infections and reinfections or persistent infections with Chlamydia trachomatis to define appropriate screening intervals and to identify risk factors for reinfection. DESIGN: This was a cross-sectional study among a subsample of participants in a population-based screening. SETTING: This study was conducted in urban and rural areas in The Netherlands. PARTICIPANTS: A total of 21,000 15- to 29-year-old women and men were invited for home-based urine testing. One year after the study, a subsample of 299 participants were offered retesting. MAIN OUTCOME MEASURES: The authors studied the rate of infection with C. trachomatis. Serovar determination was used to potentially discriminate between new infections and reinfections or persistent infections. RESULTS: Nine C. trachomatis infections were found among 187 responders (4.8% confidence interval, 1.7-7.9). The prevalence was 10.4% (5 of 48) in previous positives and 2.9% (4 of 139) in negatives. Three of 5 repeatedly positive participants were infected with a different C. trachomatis serovar. CONCLUSIONS: Our study indicates that infected persons found in a systematic, population-based screening should be re-screened within 1 year. Optimal screening intervals still need to be determined.

Adolescent↗
PubMed2005

The rate of serious bacterial infections among HIV-infected children with immune reconstitution who have discontinued opportunistic infection prophylaxis.

OBJECTIVE: Receipt of highly active antiretroviral therapy is associated with a decrease in the incidence of opportunistic infections (OIs) among HIV-infected adults. The goal of Pediatric AIDS Clinical Trials Group protocol 1008 was to evaluate prospectively the incidence of serious bacterial infections (SBIs) and other OIs after discontinuation of OI and/or Pneumocystis jiroveci pneumonia (PCP) prophylaxis among HIV-infected pediatric subjects who experienced immune reconstitution while receiving stable antiretroviral therapy. METHODS: HIV-infected children and adolescents, 2 to 21 years of age, who had received OI and/or PCP prophylaxis for > or =6 months were enrolled if they had sustained responses (>16 weeks before study entry) to antiretroviral therapy, with CD4+ cell percentages of > or =20% for patients >6 years of age or > or =25% for patients 2 to 6 years of age. Prophylaxis was discontinued at entry. To identify whether any correlation existed between functional immune reconstitution and protection from OIs, subjects were immunized with the hepatitis A virus vaccine. The association between the humoral immune response and the likelihood of developing an OI was evaluated. RESULTS: A total of 235 HIV-infected subjects from 43 participating sites had a median follow-up period of 132 weeks, yielding 547 person-years of observation. Twenty SBIs were observed among 19 subjects, resulting in an incidence rate of 3.66 SBIs per 100 person-years (95% confidence interval: 2.24-5.66 SBIs per 100 person-years). Sixteen of the events were presumed bacterial pneumonia, with 4 proven SBIs. One participant experienced 2 separate pneumonia episodes, of presumed bacterial cause. Ten subjects who developed SBIs had baseline CD4+ cell counts of > or =750 cells per mm3, and 15 had CD4+ cell percentages of > or =25% at the time of their SBIs. Two subjects died as a result of non-SBI-related causes. There were no statistically significant differences in changes over time in CD4+ cell counts or CD4+ cell percentages between subjects who experienced primary end points and those who did not. There was no evidence that baseline protease inhibitor use, gender, race/ethnicity, age, or CD4+ cell count or percentage affected the time to development of a SBI. CONCLUSIONS: OI or PCP prophylaxis can be withdrawn safely for HIV-infected pediatric patients who experience CD4+ cell recovery while receiving stable antiretroviral therapy. More studies are needed to assess the association between antibody responses to neoantigens and the development of SBIs.

AIDS-Related Opportunistic Infections↗
PubMed1997

Osteoarticular bacterial infections are rare in HIV-infected patients. 14 cases found among 4,023 HIV-infected patients.

Among 4,023 HIV-infected patients admitted to a large Italian university hospital in the period 1985-1996, 14 had concomitant HIV and bacterial osteoarticular infections. Staphylococcus aureus infections were commonest and were diagnosed in 8 patients. Intravenous drug addiction was the only risk factor significantly associated with the development of osteoarticular infection (p = 0.04). In contrast, no statistical correlations were found with age, sex, absolute number of circulating T-CD4+ lymphocytes, neutrophils and stage of HIV infection. In conclusion, osteoarticular infections are uncommon in HIV-infected patients and are more directly related to parenteral drug abuse than to HIV.

Adult↗
PubMed1978

Bovine respiratory syncytial virus infection of bovine embryonic lung cultures: enhancement of infectivity with diethylaminoethyl-dextran and virus-infected cells.

The effects of incorporating diethylaminoethyl-dextran (DEAE-D) in the inoculum with bovine respiratory syncytial virus (BRSV) on the infectivity of BRSV was evaluated. A concentration of 40 microgram DEAE-D/ml provided maximal enhancement of infection as determined by the time of onset of cytopathic effect (CPE), the percentage of cells infected by the inoculum, and the amount of virus produced. When DEAE-D was used in the inoculum, the CPE appeared a day earlier, the percentage of cells infected by the inoculum, as determined by the fluorescent antibody test, was increased 11 times, and the viral titer was increased 2 times as compared to results obtained without DEAE-D. Bovine respiratory syncytial virus-infected cultures contained much cell-associated virus which could be liberated by sonication to increase the titer of virus stocks. The use of BRSV-infected cells rather than supernates from BRSV-infected cells increased the rate at which a cytopathic effect developed, although it did not substantially increase the titer of virus which was harvested. The use of DEAE-D in the inoculum and the passage of BRSV-infected cells instead of viral suspensions was found to be the quickest and most effective method of consistently obtaining BRSV with a titer of about 10(5.5) TCID50/ml.

Animals↗
PubMed1966

Persistent infection of cells in culture by measles virus. II. Effect of measles antibody on persistently infected HeLa sublines and recovery of a HeLa clonal line persistently infected with incomplete virus.

Rustigian, Robert (Tufts University School of Medicine, Boston, Mass.). Persistent infection of cells in culture by measles virus. II. Effect of measles antibody on persistently infected HeLa clonal line persistently infected with incomplete virus. J. Bacteriol. 92:1805-1811. 1966.-The effect of viral antibody on persistent infection of HeLa cells by the Edmonston strain of measles virus was investigated by culturing cells from three persistently infected clones in medium supplemented with human immune globulin. The three infected HeLa clones were isolated from a persistently infected parent line. Two sublines which were grown in the presence of measles antibody developed a nonyielder state, wherein there is no detectable virus infectious for normal HeLa cultures. There is, however, continued synthesis of intracellular viral antigen and formation of viral intracytoplasmic inclusion bodies. The development of a nonyielder state was associated with a marked decrease in the degree of hemadsorption in cultures of both sublines. Further studies of the viral properties of non-yielder HeLa cell populations were made with a clone obtained from one of these sublines by plating under antibody. Persistent infection in this line was characterized by synthesis of incomplete virus even when the cells were cultured thereafter in anti-body-free medium. This was evidenced by (i) failure to recover infectious virus from the clonal population despite continued formation of intracellular viral antigen and viral intracytoplasmic inclusion bodies in a majority of the cells, (ii) the presence of only a few cells with surface viral antigen(s) including hemagglutinin, and (iii) the relatively weak antibody response to viral envelope antigen(s) after injection of cells into guinea pigs.

Animals↗
PubMed1992

Course of antibody production by the DIG-ELISA method in neonatally infected and juvenile infected rats after primary infection with Breinlia booliati (Filarioidea: Onchocercidae).

The course of antibody production in Wistar neonatal and juvenile rats after primary infection with Breinlia booliati was studied by the DIG-ELISA technique using filter papers impregnated with capillary blood drawn from the infected rat tails at 7, 14, 28, 60 and 90 days post infection. Sera of neonatally infected rats did not react with adult worm antigen until day 7 and the titers of antibody remained at very low levels for the next 7 days. There was little tendency to eliminate the filarial larvae during this time. The antibody levels then rose rapidly throughout the next fortnight and increased to a maximum at day 60 after which the titer leveled out at a constant high value until early patency at day 90. On the other hand, antibodies could be detected in sera of juvenile infected rats as early as day 7 and the levels of antibody rose markedly to a maximum at day 28. During the period from day 60 to day 90 at early patency, the antibodies declined gradually to lower levels. The humoral immune responses of 42 neonatally infected rats and 53 juvenile infected rats of 3 strains (Lewis, Wistar and Sprague Dawley) were tested against soluble B. booliati antigens from both female (1:50) and male (1:10) worm extracts by the DIG-ELISA method. Antibodies were detected in sera from all the microfilaremic and amicrofilaremic rats belonging to neonatally and juvenile infected groups. Sera of clean neonatal rats did not give a positive reaction zone.

Age Factors↗