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Alexander Klimov

Publications and source records attributed to Alexander Klimov.

At least 19 recordsLinked to original sources

Characterization of the epidemic influenza B viruses isolated during 2004-2005 season in Taiwan.

To characterize the antigenic and genetic relationships of influenza B viruses isolated during the 2004-2005 season, a total of 11,707 clinical respiratory samples were tested of which 1572 (13.5%) were positive for influenza (463 type A and 1109 type B influenza). Of the type B viruses, 348 isolates collected in different parts of Taiwan were further analyzed. Viruses belonging to both influenza B lineages, B/Yamagata/16/88 (B/Yam) and B/Victoris/2/87 (B/Vic) were detected, although an increasing number of B/Vic lineage isolates was obtained as the season progressed. Recent B/Vic-lineage isolates were found to have additional amino acid substitutions compared to isolates from previous seasons, indicating that viruses of this lineage continue to evolve significantly and may have the capacity to become the dominant influenza B viruses worldwide. Results presented in this report demonstrate that antigenically and genetically distinct viruses within both B/Vic and B/Yam lineages co-circulate and that reassortment among these two lineages occurs frequently contributing to the genetic diversity of the circulating strains.

Amino Acid Substitution↗

Three Indonesian clusters of H5N1 virus infection in 2005.

BACKGROUND: Since 2003, the widespread ongoing epizootic of avian influenza A (H5N1) among poultry and birds has resulted in human H5N1 cases in 10 countries. The first case of H5N1 virus infection in Indonesia was identified in July 2005. METHODS: We investigated three clusters of Indonesian cases with at least two ill persons hospitalized with laboratory evidence of H5N1 virus infection from June through October 2005. Epidemiologic, clinical, and virologic data on these patients were collected and analyzed. RESULTS: Severe disease occurred among all three clusters, including deaths in two clusters. Mild illness in children was documented in two clusters. The median age of the eight patients was 8.5 years (range, 1 to 38). Four patients required mechanical ventilation, and four of the eight patients (50%) died. In each cluster, patients with H5N1 virus infection were members of the same family, and most lived in the same home. In two clusters, the source of H5N1 virus infection in the index patient was not determined. Virus isolates were available for one patient in each of two clusters, and molecular sequence analyses determined that the isolates were clade 2 H5N1 viruses of avian origin. CONCLUSIONS: In 2005 in Indonesia, clusters of human infection with clade 2 H5N1 viruses included mild, severe, and fatal cases among family members.

Adult↗

Immunogenicity and reactogenicity of 1 versus 2 doses of trivalent inactivated influenza vaccine in vaccine-naive 5-8-year-old children.

BACKGROUND: Two doses of trivalent inactivated influenza vaccine (TIV) are recommended for children <9 years old receiving vaccine for the first time, but compliance is suboptimal. This study assessed the need for a second dose of TIV in this age group. METHODS: In this prospective, open-label study, 232 influenza vaccine-naive 5-8-year-olds enrolled in a health maintenance organization received 2 doses of TIV in fall 2004. Serum for antibody titer measurement was obtained at 3 time points (n = 222). Parents completed diaries for 5 days. RESULTS: Both doses of vaccine were well tolerated. The strongest predictor of a protective antibody response (> or =1 : 40) after 1 dose of TIV was baseline seropositive status. In multivariate analysis adjusting for age, sex, and baseline serostatus, the proportion of children with protective antibody responses was significantly higher after 2 doses than after 1 dose of TIV for each antigen (P < .001, for A/H1N1; P = .01, for A/H3N2; P < .001, for B). Age and sex were not independently predictive of a protective antibody response. Over one-third of children had antibody responses <1:40 for the type B vaccine component, even after 2 doses. CONCLUSIONS: The present study supports the need for 2 doses of TIV in 5-8-year-olds receiving TIV for the first time. Efforts to increase compliance with the 2-dose recommendation are warranted.

Antibodies, Viral↗

Histopathologic and immunohistochemical features of fatal influenza virus infection in children during the 2003-2004 season.

BACKGROUND: The Centers for Disease Control and Prevention enhanced national surveillance for influenza-associated deaths among children because of early reports of pediatric deaths during the 2003-2004 influenza season. METHODS: We studied lung and upper airway specimens from 47 case patients who died who had at least 1 positive result for influenza virus tests using hematoxylin and eosin, special stains for bacteria and fungi, and immunohistochemical (IHC) assays for influenza A and B viruses and other potential viral and bacterial respiratory pathogens. RESULTS: Nineteen (40%) of the 47 patients were <or=2 years old, and 26 (55%) were female. Influenza IHC testing identified type A antigens in 26 patients and type B antigens in 1 patient. Influenza antigens were observed focally in bronchoepithelial cells and mucous glands of trachea, bronchi, and larger bronchioli, showing submucosal mononuclear inflammatory infiltrates. IHC assays were the only confirmatory diagnostic test for 5 patients (11%). Significant life-threatening pathological conditions that could be considered the cause of death were present in 36 patients (77%) and included diffuse alveolar damage (12 cases), extensive secondary pneumonia (11 cases), extensive intraalveolar hemorrhage (10 cases), viral pneumonitis (10 cases), myocarditis (6 cases), and meningoencephalitis (1 case). For 9 patients with bronchopneumonia, a bacterial or fungal etiology was determined with IHC assay (3 Staphylococcus infections, 3 group A streptococci infections, 1 Streptococcus pneumoniae infection, 1 Bordetella pertussis infection, and 1 Aspergillus infection). CONCLUSIONS: IHC assays are useful for the diagnosis of influenza and bacterial pneumonia. This study underscores the importance of performing autopsies to identify the causes of death in patients with influenza infection.

Adolescent↗

Cross-protective immunity in mice induced by live-attenuated or inactivated vaccines against highly pathogenic influenza A (H5N1) viruses.

Because of the time required to identify and produce an antigenically well-matched pandemic vaccine, vaccines that offer broader cross-reactive immunity and protection are desirable. We have compared a live attenuated influenza vaccine (LAIV) and inactivated influenza vaccine (IIV) based on a related H5 hemagglutinin (HA) from a nonpathogenic avian influenza virus, A/Duck/Pottsdam/1042-6/86 (H5N2), for the ability to induce cross-reactive immunity and/or cross-protective efficacy against a contemporary highly pathogenic H5N1 viruses. Both LAIV and IIV provided cross-protection from systemic infection, severe disease, and death following lethal challenges with antigenically distinct A/Vietnam/1203/2004 (VN/1203) virus. Substantial levels of serum anti-VN/1203 HA IgG were detected in mice that received either IIV or LAIV, while nasal wash anti-VN/1203 HA IgA was detected in mice that received LAIV. Formulation of IIV with alum adjuvant augmented neutralizing antibody responses and protective efficacy. These results demonstrated that vaccination of mice with H5 IIV or LAIV induced a high degree of cross-protection from illness and death following lethal challenges with a heterologous H5N1 virus.

Animals↗

Detection of influenza viruses resistant to neuraminidase inhibitors in global surveillance during the first 3 years of their use.

Emergence of influenza viruses with reduced susceptibility to neuraminidase inhibitors (NAIs) develops at a low level following drug treatment, and person-to-person transmission of resistant virus has not been recognized to date. The Neuraminidase Inhibitor Susceptibility Network (NISN) was established to follow susceptibility of isolates and occurrence of NAI resistance at a population level in various parts of the world. Isolates from the WHO influenza collaborating centers were screened for susceptibilities to oseltamivir and zanamivir by a chemiluminescent enzyme inhibition assay, and those considered potentially resistant were analyzed by sequence analysis of the neuraminidase genes. During the first 3 years of NAI use (1999 to 2002), 2,287 isolates were tested. Among them, eight (0.33%) viruses had a >10-fold decrease in susceptibility to oseltamivir, one (0.22%) in 1999 to 2000, three (0.36%) in 2000 to 2001, and four (0.41%) in 2001 to 2002. Six had unique changes in the neuraminidase gene compared to neuraminidases of the same subtype in the influenza sequence database. Although only one of the mutations had previously been recognized in persons receiving NAIs, none were from patients who were known to have received the drugs. During the 3 years preceding NAI use, no resistant variants were detected among 1,054 viruses. Drug use was relatively stable during the period, except for an approximate 10-fold increase in oseltamivir use in Japan during the third year. The frequency of variants with decreased sensitivity to the NAIs did not increase significantly during this period, but continued surveillance is required, especially in regions with higher NAI use.

Antiviral Agents↗

Influenza-associated deaths among children in the United States, 2003-2004.

BACKGROUND: Although influenza is common among children, pediatric mortality related to laboratory-confirmed influenza has not been assessed nationally. METHODS: During the 2003-2004 influenza season, we requested that state health departments report any death associated with laboratory-confirmed influenza in a U.S. resident younger than 18 years of age. Case reports, medical records, and autopsy reports were reviewed, and available influenza-virus isolates were analyzed at the Centers for Disease Control and Prevention. RESULTS: One hundred fifty-three influenza-associated deaths among children were reported by 40 state health departments. The median age of the children was three years, and 96 of them (63 percent) were younger than five years old. Forty-seven of the children (31 percent) died outside a hospital setting, and 45 (29 percent) died within three days after the onset of illness. Bacterial coinfections were identified in 24 of the 102 children tested (24 percent). Thirty-three percent of the children had an underlying condition recognized to increase the risk of influenza-related complications, and 20 percent had other chronic conditions; 47 percent had previously been healthy. Chronic neurologic or neuromuscular conditions were present in one third. The mortality rate was highest among children younger than six months of age (0.88 per 100,000 children; 95 percent confidence interval, 0.52 to 1.39 per 100,000). CONCLUSIONS: A substantial number of influenza-associated deaths occurred among U.S. children during the 2003-2004 influenza season. High priority should be given to improvements in influenza-vaccine coverage and improvements in the diagnosis and treatment of influenza to reduce childhood mortality from influenza.

Adolescent↗

Evolution of the receptor binding phenotype of influenza A (H5) viruses.

Receptor specificity of influenza A/H5 viruses including human 2003-04 isolates was studied. All but two isolates preserved high affinity to Sia2-3Gal (avian-like) receptors. However, two isolates (February, 2003, Hong Kong) demonstrated decreased affinity to Sia2-3Gal and moderate affinity to a Sia2-6Gal (human-like) receptors. These two viruses had a unique Ser227-Asn change in the hemagglutinin molecule. Thus, a single amino acid substitution can significantly alter receptor specificity of avian H5N1 viruses, providing them with an ability to bind to receptors optimal for human influenza viruses. Asian 2003-04 H5 isolates from chickens and humans demonstrated highest affinity to the sulfated trisaccharide Neu5Acalpha2-3Galbeta1-4(6-HSO3)GlcNAcbeta (Su-3'SLN) receptor but, in contrast to 1997 isolates, had increased affinity to fucosylated Su-3'SLN. American poultry H5 viruses also had increased affinity to Su-3'SLN. These data demonstrate that the genetic evolution of avian influenza A(H5N1) viruses is accompanied during adaptation to poultry by the evolution of their receptor specificity.

Amino Acid Sequence↗

Isolation and characterization of avian influenza viruses, including highly pathogenic H5N1, from poultry in live bird markets in Hanoi, Vietnam, in 2001.

Since 1997, outbreaks of highly pathogenic (HP) H5N1 and circulation of H9N2 viruses among domestic poultry in Asia have posed a threat to public health. To better understand the extent of transmission of avian influenza viruses (AIV) to humans in Asia, we conducted a cross-sectional virologic study in live bird markets (LBM) in Hanoi, Vietnam, in October 2001. Specimens from 189 birds and 18 environmental samples were collected at 10 LBM. Four influenza A viruses of the H4N6 (n = 1), H5N2 (n = 1), and H9N3 (n = 2) subtypes were isolated from healthy ducks for an isolation frequency of over 30% from this species. Two H5N1 viruses were isolated from healthy geese. The hemagglutinin (HA) genes of these H5N1 viruses possessed multiple basic amino acid motifs at the cleavage site, were HP for experimentally infected chickens, and were thus characterized as HP AIV. These HA genes shared high amino acid identities with genes of other H5N1 viruses isolated in Asia during this period, but they were genetically distinct from those of H5N1 viruses isolated from poultry and humans in Vietnam during the early 2004 outbreaks. These viruses were not highly virulent for experimentally infected ducks, mice, or ferrets. These results establish that HP H5N1 viruses with properties similar to viruses isolated in Hong Kong and mainland China circulated in Vietnam as early as 2001, suggest a common source for H5N1 viruses circulating in these Asian countries, and provide a framework to better understand the recent widespread emergence of HP H5N1 viruses in Asia.

Animals↗

Neuraminidase inhibitor susceptibility network position statement: antiviral resistance in influenza A/H5N1 viruses.

The emerging epidemic of H5N1 avian influenza virus with spillover into the human population in Asia has provoked intense concern globally about the potential of these particularly pathogenic viruses to evolve with the capacity for human-to-human transmission with a consequent pandemic. The availability of antiviral drugs with activity against influenza A viruses and the recognition of drug-resistant variants to these drugs prompted the following report by a select group of the global experts--members of the Neuraminidase Inhibitor Susceptibility Network--on the best use of the available drugs, both for prophylaxis and treatment. The editors of Antiviral Therapy are pleased to be able to provide this document in an expeditious manner.

Acetamides↗

Genetic analysis of human H2N2 and early H3N2 influenza viruses, 1957-1972: evidence for genetic divergence and multiple reassortment events.

Phylogenic analysis of all gene segments of human H2N2 viruses isolated from 1957 to 1968 was undertaken to better understand the evolution of this virus subtype. Human H3N2 viruses isolated from 1968 to 1972 were also examined to investigate genetic events associated with their emergence in humans and to identify the putative H2N2 ancestral virus. All gene segments of human H2N2 viruses demonstrated divergent evolution into two distinct clades (I and II) among late H2N2 isolates. All gene segments of 1968 H3N2 viruses that were retained from human H2N2 viruses were most similar to clade I H2N2 genes. However, genes of both clades were found among H3N2 isolates of 1969-1971. Unique phylogenic topologies reflected multiple reassortment events among late H2N2 or H3N2 viruses that resulted in a variety of different genome constellations. These results suggest that H2N2 viruses continued to circulate after 1968 and that establishment of H3N2 viruses in humans was associated with multiple reassortment events that contributed to their genetic diversity.

Amino Acid Sequence↗

Reassortment and evolution of current human influenza A and B viruses.

During the 2001-2002 influenza season, human influenza A (H1N2) reassortant viruses were detected globally. The hemagglutinin (HA) of these H1N2 viruses was similar to that of the A/New Caledonia/20/99 (H1N1) vaccine strain both antigenically and genetically, while their neuraminidase (NA) was antigenically and genetically related to that of recent human influenza H3N2 reference viruses such as A/Moscow/10/99. All six internal genes of the H1N2 reassortants originated from an H3N2 virus. After being detected only in eastern Asia during the past 10 years, Influenza B/Victoria/2/87 lineage viruses reappeared in many countries outside of Asia in 2001. Additionally, reassortant influenza B viruses possessing an HA similar to that of B/Shandong/7/97, a recent B/Victoria/2/87 lineage reference strain, and an NA closely related to that of B/Sichuan/379/99, a recent B/Yamagata/16/88 lineage reference strain, were isolated globally and became the predominant influenza B epidemic strain. The current influenza vaccine is expected to provide good protection against H1N2 viruses because it contains A/New Caledonia/20/99 (H1N1) and A/Panama/2007/99 (H3N2) like viruses whose H1 HA or N2 NA are antigenically similar to those of recent circulating H1N2 viruses. On the other hand, widespread circulation of influenza B Victoria lineage viruses required inclusion of a strain from this lineage in influenza vaccines for the 2002-2003 season.

Evolution, Molecular↗

Surveillance of influenza isolates for susceptibility to neuraminidase inhibitors during the 2000-2002 influenza seasons.

Neuraminidase (NA) inhibitors (NI) have recently been licensed for the prophylaxis and treatment of influenza virus infection in humans. This study has utilized a new chemiluminescent (CL) neuraminidase assay to routinely monitor more than a thousand influenza field isolates collected worldwide during the 2000-2002 seasons for susceptibility to both licensed NIs, zanamivir, and oseltamivir by determining the 50% inhibitory concentration (IC50). Our data demonstrated that influenza A viruses of the N2 subtype were less susceptible to zanamivir, but not oseltamivir, than those of the N1 subtype such that 41 of 45 confirmed H1N2 isolates could be reliably differentiated from H1N1 viruses based on their zanamivir susceptibility. Pre-titration of influenza A viruses appeared to have no effect on IC50 determined for either NI, while pre-titration of influenza B viruses significantly reduced oseltamivir IC50 and increased zanamivir IC50. Influenza B viruses were less susceptible to either compound than type A isolates. The CL assay is a rapid and reliable method for screening large numbers of influenza isolates for NI susceptibility. Reassortant viruses of the H1N2 subtype that started to circulate worldwide during the 2001-2002 season can be reliably separated from H1N1 viruses based on their zanamivir susceptibility, enabling large scale screening of H1 isolates for determining the prevalence of such reassortants.

Acetamides↗

SARS surveillance during emergency public health response, United States, March-July 2003.

In response to the emergence of severe acute respiratory syndrome (SARS), the United States established national surveillance using a sensitive case definition incorporating clinical, epidemiologic, and laboratory criteria. Of 1,460 unexplained respiratory illnesses reported by state and local health departments to the Centers for Disease Control and Prevention from March 17 to July 30, 2003, a total of 398 (27%) met clinical and epidemiologic SARS case criteria. Of these, 72 (18%) were probable cases with radiographic evidence of pneumonia. Eight (2%) were laboratory-confirmed SARS-coronavirus (SARS-CoV) infections, 206 (52%) were SARS-CoV negative, and 184 (46%) had undetermined SARS-CoV status because of missing convalescent-phase serum specimens. Thirty-one percent (124/398) of case-patients were hospitalized; none died. Travel was the most common epidemiologic link (329/398, 83%), and mainland China was the affected area most commonly visited. One case of possible household transmission was reported, and no laboratory-confirmed infections occurred among healthcare workers. Successes and limitations of this emergency surveillance can guide preparations for future outbreaks of SARS or respiratory diseases of unknown etiology.

Adolescent↗

Assessment of development of resistance to antivirals in the ferret model of influenza virus infection.

We attempted to develop in vivo resistance of influenza virus to amantadine and to zanamivir, by use of the ferret model of influenza virus infection. Resistance of influenza virus A/LosAngeles/1/87 (H3N2) to amantadine was generated within 6 days, during a single course of treatment, and mutations in the M2 gene that are characteristic of human infections were observed. In contrast, during an identical single course of treatment with zanamivir, no evidence of reduced susceptibility was demonstrated. Pooled virus shed by zanamivir-treated ferrets was used to infect another group of ferrets. Twenty virus clones grew in plaque assays containing zanamivir, indicating possible reduced susceptibility; however, none exhibited reduced susceptibility to zanamivir in neuraminidase (NA) inhibition assays. Sequencing of the NA gene of these clones revealed only a noncoding nucleotide mutation at position 685. Sequencing of the hemagglutinin gene revealed mutations at positions 53, 106, 138, 145, 166, and 186. Similar to the situation in humans, amantadine use in ferrets rapidly produces antiviral resistance, but zanamivir use does not, although nucleotide changes were observed.

Amantadine↗

Reappearance and global spread of variants of influenza B/Victoria/2/87 lineage viruses in the 2000-2001 and 2001-2002 seasons.

Two antigenically and genetically distinct lineages of influenza B viruses, represented by the reference strains B/Victoria/2/1987 and B/Yamagata/16/1988, have cocirculated in humans since at least 1983. Between 1992 and 2000, Victoria lineage viruses were detected only in eastern Asia. From March to September of 2001 and during the 2001-2002 influenza season, Victoria lineage viruses were detected for the first time in a decade in several countries including Canada, USA, Italy, Netherlands, Norway, Philippines, India, and Oman. Phylogenetic analysis of the hemagglutinin (HA) gene of these viruses revealed that the viruses fell into two distinct clades: one group, represented by the reference strain B/Hong Kong/330/2001, contained viruses sharing three signature amino acids, Arg116, Asn121, and Glu164, while the other group of viruses, represented by B/Oman/16296/2001, shared Thr121 compared to the previous reference strain, B/Shandong/7/97. A number of the viruses in the latter group have been found to be reassortants having a Victoria lineage HA and a Yamagata lineage NA. In the current 2001-2002 season, Victoria-like viruses have now been associated with outbreaks in Asia, Europe, and North America. The reemergence of these Victoria lineage viruses worldwide, the fact that the majority of the B/Victoria-like isolates have poor cross-reactivity to B/Sichuan/379/99-like viruses in current vaccines, and the lack of exposure of young children in many areas of the world to these viruses has resulted in a World Health Organization Northern Hemisphere recommendation for the inclusion of a B/Victoria-like strain in vaccines for the 2002-2003 influenza season.

Animals↗

Surveillance for influenza--United States, 1997-98, 1998-99, and 1999-00 seasons.

PROBLEM/CONDITION: In the United States, influenza epidemics occur nearly every winter and are responsible for substantial morbidity and mortality, including an average of approximately 114,000 hospitalizations and 20,000 deaths/year. REPORTING PERIOD: This report summarizes both actively and passively collected U.S. influenza surveillance data from October 1997 through September 2000. DESCRIPTION OF SYSTEM: During each October-May in the period covered, CDC received weekly reports from 1) approximately 120 World Health Organization (WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States regarding influenza virus isolations; 2) approximately 230, 375, and 430 sentinel physicians during 1997-98, 1998-99, and 1999-00, respectively, regarding their total number of patient visits and the number of visits for influenza-like illness (ILI); and 3) state and territorial epidemiologists regarding estimates of local influenza activity. WHO collaborating laboratories also submitted influenza isolates to CDC for antigenic analysis. Throughout the year, the vital statistics offices in 122 cities reported weekly on deaths related to pneumonia and influenza (P&I). RESULTS: During the 1997-98 influenza season, influenza A(H3N2) was the most frequently isolated influenza virus type/subtype. Influenza A(H1N1) and B viruses were reported infrequently. The proportion of respiratory specimens testing positive for influenza peaked at 28% in late January. The longest period of sustained excess mortality (when the percentage of deaths attributed to P&I exceeded the epidemic threshold) was 10 consecutive weeks. P&I mortality peaked at 9.8% in January. Visits for ILI to sentinel physicians exceeded baseline levels for 7 weeks and peaked at 5% in mid-January through early February. A total of 45 state epidemiologists reported regional or widespread activity at the peak of the season. During the 1998-99 season, influenza A(H3N2) viruses predominated; however, influenza B viruses were also identified throughout the United States. Influenza A(H1N1) viruses were identified rarely. The proportion of respiratory specimens testing positive for influenza peaked at 28% in early February. P&I mortality exceeded the epidemic threshold for 12 consecutive weeks and peaked at 9.7% in early March. Visits for ILI to sentinel physicians exceeded baseline levels for 7 weeks and peaked at 5% in early through mid-February. Forty-three state epidemiologists reported regional or widespread activity at the peak of the season. During the 1999-00 season, influenza A(H3N2) viruses predominated, but influenza A(H1N1) and B viruses also were identified. The proportion of respiratory specimens testing positive for influenza peaked at 31% in mid- to late December. The proportion of deaths attributed to P&I exceeded the epidemic threshold for 13 consecutive weeks and peaked at 11.2% in mid-January. Visits to sentinel physicians for ILI exceeded baseline levels 4 consecutive weeks and peaked at 6% in late December. Forty-four state epidemiologists reported regional or widespread activity at the peak of the season. INTERPRETATION: Influenza A(H1N1), A(H3N2), and B viruses circulated during 1997-2000, but influenza A(H3N2) was the most frequently reported virus type/subtype during all three seasons. Influenza A(H3N2) is the virus type/subtype most frequently associated with excess P&I mortality. Influenza activity during all three seasons occurred at moderate to severe levels, and excess P&I mortality was reported during > or = 10 weeks each year. PUBLIC HEALTH ACTIONS: CDC conducts active national surveillance during each October-May to detect the emergence and spread of influenza virus variants and to monitor influenza-related morbidity and mortality. Surveillance data are provided weekly throughout the influenza season to public health officials, WHO, and health-care providers and are used to guide vaccine strain selection, prevention and control activities, and patient care. Influenza vaccination is the most effective means for reducing the yearly effect of influenza. Typically, one or two of the influenza vaccine component viruses are updated each year so that vaccine strains will closely match circulating viruses. Surveillance data will continue to be used to select vaccine strains and to monitor the match between vaccine strains and the currently circulating viruses.

Disease Outbreaks↗

Intercontinental circulation of human influenza A(H1N2) reassortant viruses during the 2001-2002 influenza season.

Reassortant influenza A viruses bearing the H1 subtype of hemagglutinin (HA) and the N2 subtype of neuraminidase (NA) were isolated from humans in the United States, Canada, Singapore, Malaysia, India, Oman, Egypt, and several countries in Europe during the 2001-2002 influenza season. The HAs of these H1N2 viruses were similar to that of the A/New Caledonia/20/99(H1N1) vaccine strain both antigenically and genetically, and the NAs were antigenically and genetically related to those of recent human H3N2 reference strains, such as A/Moscow/10/99(H3N2). All 6 internal genes of the H1N2 reassortants examined originated from an H3N2 virus. This article documents the first widespread circulation of H1N2 reassortants on 4 continents. The current influenza vaccine is expected to provide good protection against H1N2 viruses, because it contains the A/New Caledonia/20/99(H1N1) and A/Moscow/10/99(H3N2)-like viruses, which have H1 and N2 antigens that are similar to those of recent H1N2 viruses.

Antigens, Viral↗