Infection with multiple CMV strains occurs in infants with congenital CMV infection. The impact of intrauterine infection with multiple virus strains on the pathogenesis and long-term outcome remains to be elucidated.

Infection and reinfection with multiple cytomegalovirus (CMV) strains have been shown to occur in immunocompromised individuals, sexually transmitted disease clinic attendees, and children attending day care centers. To characterize the CMV diversity in healthy seropositive individuals, 16 CMV PCR-positive specimens from 113 seropositive women were analyzed for glycoprotein gN and gB genotypes by cloning, followed by nucleotide sequencing of the plasmid DNA and/or restriction fragment length polymorphism (RFLP). The results showed that most (93.7%) of the PCR-positive specimens contained multiple gN and/or gB genomic variants, suggesting that the majority of women were infected with more than one virus strain. The results also showed that the RFLP technique might not be sufficiently sensitive to detect all of the genomic variants present in a sample.Cytomegalovirus (CMV) species are important opportunistic agents in infection of immunocompromised individuals and a frequent cause of congenital infection. Infection with multiple strains of CMV has been shown to occur frequently in immunocompromised individuals and sexually transmitted disease (STD) clinic attendees (8, 10). In addition, reinfection with different CMV strains was documented to occur in children attending day care centers (2). More recently, CMV reinfections were demonstrated in seropositive women, and such reinfections can result in intrauterine transmission and damaging fetal infection (5).Extensive genetic polymorphisms in envelope glycoproteins of CMV, including glycoprotein B (gpUL55), glycoprotein O (gpUL74), and glycoprotein N (gpUL73), have been demonstrated among clinical CMV isolates. Major envelope glycoprotein B (gB) of CMV has been demonstrated to elicit a strong neutralizing antibody response (6), and on the basis of restriction fragment length polymorphism (RFLP) analysis of clinical samples, four unique genomic variants, gB types 1 to 4, have been identified (9). Glycoprotein N has been shown to be highly polymorphic at the amino-terminal region, and most clinical CMV isolates have been shown to cluster into four distinct genomic variants, gN-1, gN-2, gN-3a, gN-3b, gN-4a, gN-4b, and gN-4c (11). Recent studies have shown that a significant proportion of the virus-neutralizing response was also directed against the gM/gN complex (17). No linkage between gN genotypes and gB genotypes has been observed (11).Published studies using RFLP analyses to determine the gN genotypes have identified only a single gN type in a given sample (11, 13). Studies of glycoprotein B based on RFLP analyses showed the presence of a single genotype or a limited number of samples containing mixtures of two gB genotypes (3, 7). However, a recent study using hybridization with typespecific probes (10) showed mixtures of all genotypes. To determine the CMV strain diversity in healthy seropositive women, the presence of multiple gN and gB genomic variants in urine or peripheral blood was examined by two different methods, RFLP and cloning followed by nucleotide se...

Testing of paired mid-turbinate (MT) nasal and nasopharyngeal (NP) swabs, collected by trained personnel from 40 patients with COVID-19 showed more NP (76/95, 80%) than MT swabs tested positive (61/95, 64%; p=0.02). Among samples collected a week after study enrollment, fewer MT than NP samples were positive (45% vs 76%; p=0.001).

To determine the incidence and natural history of congenital cytomegalovirus (CMV) infection in a population of women with near universal serologic reactivity for CMV, a prospective study of 423 women attending the antenatal clinic of the Comprehensive Rural Health Center in northern India was conducted. All 9 (2.1%) CMV positive infants were born to mothers who were CMV seropositive at the first antenatal visit. One child had hepatosplenomegaly at birth and another child had mild unilateral hearing loss at 4 months of age.

The birth prevalence of congenital CMV was high despite prenatal ARV prophylaxis, and was associated with advanced maternal immunosuppression.

Background Congenital cytomegalovirus (cCMV) is a common congenital infection and a leading non-genetic cause of sensorineural hearing loss (SNHL). CMV exhibits extensive genetic variability and infection with multiple CMV strains (mixed infection) was shown to be common in cCMV. The role of mixed infections in disease and outcome remains to be defined. Methods Genotyping of envelope glycoproteins, UL55 (gB), UL73 (gN) and UL75 (gH) was performed on saliva specimens from 79 infants from the ongoing CMV and Hearing Multicenter Screening Study (CHIMES) and on blood and urine specimens from 52 infants who participated in natural history studies at the University of Alabama at Birmingham. Genotyping of UL144 and US28 was also performed in the CHIMES cohort. The association of individual genotypes and mixed infection with clinical findings at birth and SNHL was examined. Results Thirty seven of 131 infants (28%) were symptomatic at birth and 26 (20%) had SNHL at birth. All known genotypes of UL55, UL75, UL73, and US28 were represented and no particular genotype was associated with symptomatic infection or SNHL. UL144 subtype C was more common in symptomatic babies but not associated with SNHL. Mixed infection was observed in 59 infants (45%) and not associated with symptoms (p = 0.43) or SNHL at birth (p = 0.82). In the cohort of 52 infants with long-term hearing outcome, mixed infection at birth was not predictive of SNHL. Conclusions Mixed infection is common in infants with cCMV but is neither associated with symptomatic infection nor with SNHL.

The prevalence of cCMV was low, and outcomes at 18 months of age did not differ between the infected infants and healthy control infants. With such a low burden in Finland, universal newborn screening for cCMV seems unwarranted.

Nonprimary CMV infection was common in mothers after primary infection in their infants, consistent with infant-to-mother transmission. Because infants frequently acquire CMV from their mothers, for example, through breast milk, this suggests the possibility of "ping-pong" infections. Additional research is needed to characterize the antigenic and genotypic strains transmitted among children and their mothers.